Search

Objective: To discuss the effect of curcumin on ameliorating doxorubicin (DOX) -induced cytotoxicity in the H9c2 cardiomyocytes, and to clarify its mechanism. Methods: The H9c2 cardiomyocytes were treated with DOX to establish the cardiotoxicity model. The H9c2 cells were divided into normal group, DOX group, DOX+curcumin group, and DOX+curcumin+silent information regulator 3 (SIRT3) inhibitor-3 (3-TYP) group. After 24 h, the morphology of the cells in various groups were observed; CCK-8 method was used to detect the viabilities of the cells in various groups; TUNEL staining was used to detect the apoptotic rates of the cells in various groups; enzyme-linked immunosorbent assay (ELISA) method was used to detect the activities of catalase (CAT) and superoxide dismutase (SOD) and the levels of malondialdehyde (MDA) in the cells in various groups; 2, 7-dichlorofluorescein diacetate (DCFH-DA) staining was used to detect the levels of reactive oxygen species (ROS) in the cells in various groups; Western blotting method was used to detect the expression levels of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2), NADPH oxidase 4 (NOX4), SIRT3, acetylated superoxide dismutase 2 (Ac-SOD2), and superoxide dismutase 2 (SOD2) proteins in the cells in various groups. Results: Compared with normal group, the H9c2 cells in DOX group exhibited swelling, the activity of the cells was decreased (P< 0. 05), the CAT and SOD activities were decreased (P<0. 05), the MDA and ROS levels were increased (P<0. 05), the expression levels of NOX2, and NOX4 proteins were increased (P< 0. 05), the ratio of Bcl-2/Bax and the expression level of SIRT3 protein were decreased (P<0. 05), and the expression levels of SOD2 and Ac-SOD2 proteins were increased (P<0. 05). Compared with DOX group, the H9c2 cells in DOX+curcumin group showed improved morphology, the activity of the cells was increased (P<0. 05), the CAT and SOD activities were increased (P<0. 05), the MDA and ROS levels were decreased (P<0. 05), the expression levels of NOX2, and NOX4 proteins were decreased (P< 0. 05), the ratio of Bcl-2/Bax and the expression level of SIRT3 protein were increased (P<0. 05), and the expression levels of SOD2 and Ac-SOD2 proteins were decreased (P<0. 05). Compared with DOX+ curcumin group, the cells in DOX+curcumin+3-TYP group exhibited swelling, the activity of the cells was decreased (P<0. 05), the apoptotic rate of the cells was significantly increased (P<0. 05), the CAT and SOD activities were decreased (P<0. 05), the MDA and ROS levels were significantly increased (P<0. 05), the expression levels of NOX2 and NOX4 proteins were increased (P<0. 05), the ratio of Bcl-2/Bax and the expression level of SIRT3 protein were decreased (P<0. 05), and the expression levels of SOD2 and Ac-SOD2 proteins were increased (P<0. 05). Conclusion: Curcumin suppresses the oxidative stress and apoptosis by activating the SIRT3/SOD2 signaling pathway, improving the cell activity and alleviating the DOX-induced cytotoxicity in the H9c2 cells. [ABSTRACT FROM AUTHOR]

Aim To investigate the effect of theaflavin on oxidized low density lipoprotein (ox-LDL)-induced foam cell formation and oxidative stress in THP-1 macrophages and its mechanism. Methods THP-1 derived macrophages were pretreated with 50 μmol/L theaflavin and (or) 10 μmol/L nuclear factor erythroid 2-related factor 2 (NRF2) inhibitor ML385, then 100 mg/L ox-LDL was added to the cells for 24 h to establish the foam cell model. The effect of theaflavin on THP-1 macrophages viability was evaluated by CCK-8 assay and LDH release. The expression of inflammatory cytokines interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) were analyzed by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot. The release of inflammatory cytokines were detected by enzyme linked immunosorbent assay (ELISA). Intracellular lipid accumulation was detected by Oil red O staining, and lipid absorption was observed by DiL-labeled oxidized low density lipoprotein (DiL-ox-LDL) staining. Reactive oxygen species (ROS) level was detected by DCFH-DA probe. The expression of lipid uptake, cholesterol efflux and oxidative stress-related proteins were detected by Western blot and RT-qPCR. Results Treatment with 100 mg/L ox-LDL significantly decreased cell viability and cholesterol efflux-related protein expressions, increased lipid uptake, accumulation and lipid uptake-related protein expressions, and significantly promoted inflammation and ROS level, as well as the expressions of myeloperoxidase (MPO), NADPH oxidase 2 (NOX2) in THP-1 macrophages (all P<0. 05). After pretreatment with theaflavin, cell viability was increased, intracellular lipid uptake, accumulation and lipid uptake-related protein expressions were significantly reduced, cholesterol efflux-related protein expressions were significantly increased, the expression and release of IL-6, IL-1β and TNF-α were significantly decreased, ROS level was significantly decreased, and the expression of MPO and NOX2 were decreased (all P<0. 05). Pretreatment with theaflavin effectively alleviated intracellular oxidative stress by altering the expression of NRF2, heme oxygenase-1 (HO-1) and Kelch-like ECH-associated protein 1 (KEAP1) in NRF2 signaling pathway, and enhanced the translocation of NRF2 into the nucleus. After pretreatment with ML385, the expression levels of NRF2, HO-1, KEAP1 and CD36 were significantly decreased. Conclusion Theaflavin can significantly inhibit ox-LDL-induced foam cell formation, inflammation, and oxidative stress through NRF2/HO-1 signaling pathway in THP-1 macrophages. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

] AIM: To evaluate the therapeutic effect of Shen-Xiankang formula on renal interstitial fibrosis induced by unilateral ureteral obstruction (UUO) in mice and to elucidate its underlying mechanisms. METHODS: Thirty-two C57BL/6 mice were randomly divided into sham group, UUO model group, and Shen-Xiankang formula intervention groups receiving either a low dose (150 mg'kg-l-d-1) or a high dose (450 mg'kg-l-d-1), with 8 mice in each group. All mice except those in sham group underwent UUO to establish chronic kidney disease (CKD) model. After modeling, corresponding doses of Shen-Xiankang or an equivalent volume of saline were administered daily for 7 d. Upon completion of treatment, renal tissues were collected for hematoxylin-eosin (HE) and Masson staining to assess tissue damage and fibrosis. Immunohistochemistry and Western blot analyses were used to detect the markers of fibrosis, oxidative stress, and ferroptosis. The effect of Shen-Xiankang formula on the interaction between activating transcription factor 3 (ATF3) and Smad3 was assessed using co-immunoprecipitation (Co-IP). RESULTS: The untreated UUO model group exhibited notable pathological changes such as expanded renal tubules and collagen deposition. Shen-Xiankang treatment significantly alleviated these changes (P<0. 05). It markedly reduced Smad3 phosphorylation, ATF3, 4-hydroxynonenal (4-HNE), and NADPH oxidase 4 (NOX4) aberrant expression, while increasing glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) expression. Co-IP results indicated a significant modulation of the ATF3-Smad3 interaction by Shen-Xiankang. CONCLUSION: Shen-Xiankang formula effectively mitigates UUO-induced renal interstitial fibrosis in mice. The mechanism may involve modulating the ATF3/Smad3 interaction, which in turn attenuates oxidative stress and ferroptosis, consequently leading to the amelioration of renal fibrosis. These findings provide important insights for further research and clinical application of Shen-Xiankang formula. [ABSTRACT FROM AUTHOR]

NADPH Oxidase (NOXs) is an enzyme that produces superoxide and plays an important role in organism defense, biosynthesis pathway and cell signal transduction. NOXs, as a major source of reactive oxygen species (ROS), has become a popular target for anti-oxidative stress, inflammation, fibrosis, and tumors. Literature suggests that NOXs and their related REDOX reactions are closely related to osteoclasts and osteoblasts, driving membrane-associated reactive oxygen species (ROS) and initiating iron death, affecting bone formation and bone resorption. This paper aims to review the effects of NOXs on ROS and iron death in bone homeostasis and provide references for the treatment of bone metabolism related diseases with NOXs. [ABSTRACT FROM AUTHOR]

Objective: To investigate the role of Nox2 on AngII-stimulated aldosterone biosynthesis. Methods: H295R cells were cultured and randomly divided into control group, Angll group, AngII+gp91ds-tat group, AngII+PEG-Cat group, AngII+Nox2 siRNA group. Q-PCR and western blot were performed to determine CYP1IB2 and Nox2 expression in H295R cells. Aldosterone level in cells culture supernatant was determined by radioimmunoassay. Nox2-derived ROS and H2O2 production in H295R cells were determined by flow cytometric analysis and fluorescence microplate reader. Results: 10 nmol/L Angll increased cellular ROS and H2O2 generation, increased the Nox2 and CYP11B2 expression and accelerated aldosterone biosynthesis in a time-dependent manner (P<0.05). And AngII-induced cellular ROS and H₂O, production in both AngII+gp91ds-tat and AngII+PEG-Cat groups were lower than those in AngII group (P<0.05). However, there were no difference in inhibition of cellular ROS and H2O2 between treatment with gp91ds-tat and PEG-Cat (P>0.05). The expression of CYP11B2 in H295R cells was up-regulated after treated with 10 nmol/L Angll for 24 h (P<0.05), while gp91ds-tat, PEG-Cat and Nox2 siRNA significantly abrogated the CYP11B2 expression in H295R cells (P<0.05). Conclusion: Nox2 dependent ROS play an important role in aldosterone synthesis. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the role of extracellular signal regulated kinase 1/2 （ERK1/2） in colitis through the regulation of NADPH oxidase and mitochondrial fission. Methods Mice models of acute colitis were induced by 3% dextran sulfate sodium （DSS）. Thirty C57BL/6J mice were randomly divided into six groups by random number table method： control group， 3%DSS group，1% dimethyl sulfoxide （DMSO） group， ERK1/2 inhibitor（PD98059） group， 3%DSS+1%DMSO group and 3%DSS+PD98059 group， with five mice in each group. The changes of body weight， colonic length， disease activity index and colonic histopathological changes of mice in the control and 3%DSS groups were evaluated， and the expression levels of ERK1/2， p-ERK1/2， Nicotinamide adenine dinucleotide phosphate oxidase 1 （Nox1） and Nox2 in colonic mucosa of mice were detected. Mice in 1%DMSO and 3%DSS+1%DMSO groups were intraperitoneally injected with 1%DMSO. Mice in the PD98059 and 3%DSS+PD98059 groups were intraperitoneally injected with PD98059. The colonic histopathological changes were evaluated among four groups， and the expression levels of Nox1， Nox2， Dynamin related protein 1 （DRP1）， p-DRP1-S616 and p-DRP1-S637 mitochondrial fission related proteins were detected. Mitochondrial fission of colonic epithelial cells in the control and 3%DSS groups was observed by transmission electron microscopy. The co-localization of Nox2 and mitochondrial outer membrane translocator enzyme TOM complex （TOMM20） in colonic mucosa of mice in two groups was analyzed by double-immunofluorescence staining. The correlation between relative expression levels of DRP1 and Nox2 mRNA in mouse colonic mucosa was analyzed in two groups. Results Compared with the control group， mice in the 3%DSS group exhibited body weight loss， shortened colonic length， increased disease activity index and increased colonic histopathological score. The expression levels of p-ERK1/2， Nox1， Nox2 in colonic mucosa of mice were significantly up-regulated in the 3%DSS group （all P < 0.05）. In mice with colitis， mitochondrial fission in colonic epithelial cells was increased， and the colonic mucosa co-localization of DRP1 and Nox2 was elevated， and the relative mRNA expression levels of both target genes were positively correlated （r = 0.678， P < 0.05）. ERK1/2 inhibitor PD98059 improved colonic histopathological changes in mice with colitis， and down-regulated the expression levels of Nox1， Nox2， DRP1， p-DRP1-S616 in colonic mucosa. Conclusion Inhibition of ERK1/2 may ameliorate colitis by down-regulating NADPH oxidase expression and alleviating mitochondrial fission.

AIM: To investigate the inhibitory effect of modulating nuclear factor E2-related factor 2 （Nrf2）/glutathione peroxidase 4 （GPX4） signaling pathway on ferroptosis and renal fibrosis in unilateral ureteral obstruction （UUO） mice. METHODS: The expression levels of GPX4, Nrf2 and α-smooth muscle actin（ α-SMA） were measured by immunohistochemistry in paraffin sections of kidney puncture specimens from 9 chronic kidney disease （CKD） patients and 9 non-CKD patients. In animal experiments, 25 male C57BL/6 mice （6 to 8 weeks old） were randomly divided into 5 groups: sham group, UUO group, UUO+liproxstatin-1 （Lip-1; ferroptosis inhibitor） group, UUO+sulforaphane （SFN; Nrf2 agonist） group, and UUO+irbesartan （IRB） group. The mice in each group were fed with normal chow for 1 week, and those in the latter 3 groups were intraperitoneally injected with Lip-1 （10 mg·kg-1·d-1）, SFN （25 mg·kg-1·d-1） and urea nitrogen. Kidney tissues were embedded in paraffin and stained with HE, Masson and Sirius red to observe the renal pathological changes. Western blot, RT-qPCR and immunohistochemistry were applied to determine the expression levels of Nrf2, GPX4, solute carrier family 7 member 11 （SLC7A11）, fibronectin （Fn）, collagen type I （Col-I）, α-SMA, and NADPH oxidase 4 （NOX4） in mouse kidney tissues. RESULTS: Immunohistochemical results showed that the expression levels of GPX4 and Nrf2 were lower in CKD patients than those in non-CKD patients, while the expression of α-SMA was higher than that in non-CKD patients. In animal experiments, the mice in the 3 treatment groups had improved renal function, reduced fibrosis, and decreased expression of renal fibrosis-related indexes compared with UUO group. The expression levels of Nrf2, GPX4 and SLC7A11 in renal tissues of Lip-1 and SFN treatment groups were higher than those of UUO group（ P<0. 05）, while the expression of NOX4 was lower than that of UUO group（ P<0. 05）. CONCLUSION: Fibrosis and ferroptosis were significantly increased in the kidneys of CKD patients and UUO mice. Regulation of Nrf2/GPX4 signaling pathway could effectively inhibit ferroptosis and attenuate kidney fibrosis in UUO mice. [ABSTRACT FROM AUTHOR]

To understand the cytological mechanism of allelopathy of Eucalyptus robusta, the toxic effects of volatiles from E. robusta were studied by microscopic, cytochemical and qRT-PCR techniques, taking volatile oil from E. robusta and its main components α-pinene and eucalyptol as donors, and using root cells and leaf guard cells of Vicia faba as targets. The results were as follows: (1) The growth of radicle of V. faba were exhibited and showed a time-concentration dependent effects under the treatments of the volatiles of Eucalyptus robusta. The allelopathic effects were volatile oil, a-pinene and eucalyptol in descending order. (2) When Vicia faba roots were exposed to Eucalyptus robusta volatiles, the activity of root border cells decreased, the micronucleus rate of cells in the meristematic zone increased, mitotic index decreased, and the cell cycle of most cells was arrested in the prophase of division. (3) Under the action of the volatiles of E. robusta, the activity of NADPH oxidase increased, reactive oxygen species (ROS) burst in leaf guard cells of Vicia faba, microfilament polymerization, and stomatal aperture decreased. At the same time, the leaf epidermis strip of V. faba was treated with Eucalyptus robusta volatiles, the nuclear distortion rate of leaf guard cells increased. Moreover, the treatment of E. robusta volatiles led to the decrease of guard cell activity and caspase-dependent apoptosis in Vicia faba. However, the guard cell survival rates increased when the leaf epidermis strips of V. faba were exposed to volatiles from Eucalyptus robusta combined with different concentrations of Ca channel blocker (LaCl3), ROS scavenger ascorbic acid (ASA), and nitrate reductase inhibitors (NaN3), which indicated that the volatiles of E. robusta changed the signal regulation of Ca2+, ROS and NO. These results suggested that the cytotoxicity and genotoxicity of the volatiles of E. robusta altered the signal transduction pathway of the receptor cells, induced the genetic aberration of the root tip cells, then led to the dysfunction of protective function and stomatal movement of the receptor root border cells, which affected the root growth and photosynthesis of the receptor, and ultimately hindered the growth of receptor. The results provide a theoretical basis for scientific planting and management of E. robusta planting area. [ABSTRACT FROM AUTHOR]

Copyright of Food Research & Development is the property of Food Research & Development Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

【Objective】To explore the allelopathy mechanism of Eucalyptus globulus and E. grandis, the effects of two volatile oils from Eucalyptus leaf and their two common components, alpha-pinene and eucalyptol, the physiological changes of root border cells and leaf guard cells of Vicia faba L. and the signal regulation in guard cells were studied to explore the allelopathic mechanism of the two eucalyptus species. 【Method】 The activity of root border cells and leaf guard cells and stomatal aperture and the regulation of ROS, NO and Ca2+ signal molecules in guard cells by different volatile oils and their common components α-Concentration of pinene and cineole(2,4,6,8 and 10 μL) were studied by using microscopy technology, cytochemistry mothed and qRT-PCR. 【Result】With the increase of the treatment dose of volatile oil, α-pinene and eucalyptol, the activities of root border cells and leaf guard cells decreased gradually. The NADPH oxidase gene in leaves was up-regulated, the levels of intracellular signaling molecules such as ROS, NO, Ca2+ were increased and various nuclear aberrations appeared in guard cells. TUNEL results showed that the guard cells died in the form of apoptosis. The guard cells mortality was decreased when the volatiles were combined with Z-VAD-FMK(a pan-Caspase inhibitor), LaCl3(a specific calcium-channel blocker), ascorbic acid(AsA, a reactive oxygen scavenger) and NaN3(a nitrate reductase inhibitor). In situ observation of ROS, NO and Ca2+ showed that compared with volatile oil treatment group, the levels of NO and Ca2+ in volatiles and AsA co-treated group were lower, and the levels of ROS and Ca2+ in volatiles and NaN3 co-treated group were lower, and there was no significant difference in ROS and no levels in volatiles and LaCl3 co-treated group. The results showed that the crosstalk between ROS and NO led to the increase of Ca2+ concentration in guard cells, which triggered Ca2+-dependent and Caspase-dependent apoptosis. In addition, the stomatal aperture decreased with the increase of the treatment dose of Eucalyptus volatiles. The reduction of stomatal aperture caused by Eucalyptus volatiles was alleviated when microfilament polymerization inhibitor Cytochalasin B(CB), NADPH oxidase inhibitor diphenylene iodonium(DPI), active oxygen scavenger ascorbic acid(ASA) were co-treated with volatiles, indicating that ROS burst in guard cells induced microfilament polymerization and caused stomatal closure. 【Conclusion】The allelochemicals released by E. globulus and E. grandis through the volatile pathway induced oxidative damage, which damaged the structure and function of guard cells and root border cells with root protective barrier function, as well as absorption and photosynthesis processes, and receptor growth was inhibited. [ABSTRACT FROM AUTHOR]

Objective: To reveal the possible role of phosphodiesterase 2A (PDE2A) in age-related macular degeneration (AMD)and its effect on choroidal neovascularization (CNV). Methods: The serum PDE2A levels in 36 wet AMD patients (AMD group) and 36healthy subjects (Healthy group) were detected by qRT-PCR. Rhesus monkey choroidal vascular endothelial cell line (RF/6A) was divided into Normoxia group, Hypoxia group, Hypoxia+NC group and Hypoxia+PDE2A group. NC-shRNA and PDE2A-shRNA lentivirus were transfected into Hypoxia+NC group and Hypoxia+PDE2A group by Lipofectamine2000, respectively. After transfection,according to the grouping, 200 m M CoCl2was added to RPMI1640 medium to treat RF/6A cells under hypoxia. After the laser-induced CNV mouse model was established, 36 successfully modeled mice were randomly divided into model group, NC-shRNA group and PDE2A-shRNA group, with 12 mice in each group. Twelve unmodeled mice were selected as the Control group. The corresponding lentiviruses were injected into the vitreous cavity of mice in the NC-shRNA group and the PDE2A-shRNA group, respectively, for a total of 7 days of treatment. The mice were then subjected to fundus fluorescein angiography (FFA) and eye HE staining. The contents of ROS, SOD and MDA in mouse choroidal tissue were detected using corresponding kits. The expressions of PDE2A, VEGFA, VEGFR2,HIF-1α, NOX2, NOX4 and NF-κB p65 in RF/6A cells or choroidal tissues were detected by qRT-PCR or Western blot. Results: Compared with Healthy group, the serum PDE2A level in AMD group was significantly increased (1.00 ±0.23 vs 3.09±1.46, t=8.507,P＜0.001). Compared with Hypoxia group, the number of closed lumens of RF/6A cells in Hypoxia+PDE2A group decreased (P＜0.05), and the m RNA and protein expressions of PDE2A, VEGFA, VEGFR2 and HIF-1α were decreased (P＜0.05). Compared with Model group, the choroidal lesions of the CNV mice in PDE2A-shRNA group were significantly reduced, angiogenesis and choroidal hyperplasia were significantly reduced, and the relative fluorescence intensity of CNV was decreased (P＜0.05), the m RNA and protein expression levels of PDE2A, VEGFA, VEGFR2 and HIF-1α in choroidal tissue were decreased (P＜0.05). Compared with Model group, the contents of ROS and MDA in the choroidal tissue of PDE2A-shRNA group were decreased, and the content of SOD was increased (P＜0.05). Compared with Model group, the relative expressions of NOX2, NOX4 and nuclear NF-κB p65 proteins in the choroidal tissue of PDE2A-shRNA group were all decreasedcP＜0.05). Conclusion: PDE2A participates in age-related macular degeneration by affecting choroidal angiogenesis and NADPH Oxidase/ROS/NF-κB pathway. [ABSTRACT FROM AUTHOR]

Objective To investigate the role of extracellular signal regulated kinase 1/2 （ERK1/2） in colitis through the regulation of NADPH oxidase and mitochondrial fission. Methods Mice models of acute colitis were induced by 3% dextran sulfate sodium （DSS）. Thirty C57BL/6J mice were randomly divided into six groups by random number table method： control group， 3%DSS group，1% dimethyl sulfoxide （DMSO） group， ERK1/2 inhibitor（PD98059） group， 3%DSS+1%DMSO group and 3%DSS+PD98059 group， with five mice in each group. The changes of body weight， colonic length， disease activity index and colonic histopathological changes of mice in the control and 3%DSS groups were evaluated， and the expression levels of ERK1/2， p-ERK1/2， Nicotinamide adenine dinucleotide phosphate oxidase 1 （Nox1） and Nox2 in colonic mucosa of mice were detected. Mice in 1%DMSO and 3%DSS+1%DMSO groups were intraperitoneally injected with 1%DMSO. Mice in the PD98059 and 3%DSS+PD98059 groups were intraperitoneally injected with PD98059. The colonic histopathological changes were evaluated among four groups， and the expression levels of Nox1， Nox2， Dynamin related protein 1 （DRP1）， p-DRP1-S616 and p-DRP1-S637 mitochondrial fission related proteins were detected. Mitochondrial fission of colonic epithelial cells in the control and 3%DSS groups was observed by transmission electron microscopy. The co-localization of Nox2 and mitochondrial outer membrane translocator enzyme TOM complex （TOMM20） in colonic mucosa of mice in two groups was analyzed by double-immunofluorescence staining. The correlation between relative expression levels of DRP1 and Nox2 mRNA in mouse colonic mucosa was analyzed in two groups. Results Compared with the control group， mice in the 3%DSS group exhibited body weight loss， shortened colonic length， increased disease activity index and increased colonic histopathological score. The expression levels of p-ERK1/2， Nox1， Nox2 in colonic mucosa of mice were significantly up-regulated in the 3%DSS group （all P < 0.05）. In mice with colitis， mitochondrial fission in colonic epithelial cells was increased， and the colonic mucosa co-localization of DRP1 and Nox2 was elevated， and the relative mRNA expression levels of both target genes were positively correlated （r = 0.678，P < 0.05）. ERK1/2 inhibitor PD98059 improved colonic histopathological changes in mice with colitis， and down-regulated the expression levels of Nox1， Nox2， DRP1， p-DRP1-S616 in colonic mucosa. Conclusion Inhibition of ERK1/2 may ameliorate colitis by down-regulating NADPH oxidase expression and alleviating mitochondrial fission. [ABSTRACT FROM AUTHOR]

BACKGROUND: Studies have shown NADPH oxidase (NOX) protein expression will up-regulate in the myocardium, skeletal muscle, kidney, and brain under stress conditions. However, its role in alcoholic liver damage is still unclear. OBJECTIVE: To investigate the role of NOX-mediated oxidative stress in normal liver tissue and alcoholic liver damage. METHODS: (1) Six male C57BL/6J mice were randomly divided into normal control group and normal drug group, with three mice in each group. Mice in the normal drug group were intraperitoneally injected with 10 mg/kg apocynin for 4 consecutive days, while those in the normal control group were injected with the same dose of solvent. Lipid metabolism-related indexes in serum and liver tissue of mice were detected, and the protein expressions of NOX2 and NOX4 in liver tissue were determined. (2) Another 18 male C57BL/6J mice were randomly divided into common control group, alcoholic control group, alcoholic drug group, with 6 mice in each group. Mice in the common control group were given TP4030C, while those in the other two groups were given Lieber-DeCarli liquid diet to construct animal models of alcohol-induced hepatocellular injury. During the modeling, mice in the alcoholic drug group were intraperitoneally injected with 10 mg/kg apocynin, 6 days a week, for 5 continuous weeks, while those in the other two groups were injected with the same dose of solvent. (3) Body mass, epididymal fat relative mass, liver index and relative mass of the skeletal muscle were recorded or calculated. Glucose tolerance test was used to detect insulin sensitivity, and serum liver function and lipid metabolism indexes were measured. Levels of malondialdehyde, superoxide dismutase, triglycerides, highdensity lipoprotein cholesterol, and low-density lipoprotein cholesterol were determined. Pathological changes of the liver were observed using hematoxylineosin staining. Western blot assay was applied to detect NOX2 and NOX4 protein expression in liver tissue. RESULTS AND CONCLUSION: Compared with the normal control group, the content of triglycerides in liver tissue and the levels of serum alanine aminotransferase and aspartate aminotransferase in serum were significantly increased, while high-density lipoprotein cholesterol level and the expression of NOX2 and NOX4 in liver tissue decreased significantly in the normal drug group (P < 0.05 or P < 0.01). Compared with the common control group, the relative content of epididymal fat and the level of high-density lipoprotein cholesterol in both serum and liver tissue were significantly decreased in the alcoholic control group, while triglyceride and low-density lipoprotein cholesterol levels in liver tissue, serum alanine aminotransferase level and NOX4 protein expression were significantly increased in the alcoholic control group. Compared with the alcoholic control group, the alcoholic drug group had a significant increase in the high-density lipoprotein cholesterol levels in the serum and liver tissue but had a significant decrease in serum alanine aminotransferase level and low-density lipoprotein cholesterol level and NOX4 protein expression in liver tissue. In conclusion, inhibiting NOX alleviates alcohol-induced hepatocellular injury and lipid metabolism disorder; apocynin has different effects on liver physiological and pathological states of alcoholic liver damage. [ABSTRACT FROM AUTHOR]

Objective: To investigate the protective effect of ginsenoside Rg1 on cardiac injury in the rats with severe acute pancreatitis(SAP），and to elucidate the related molecular mechanisms. Methods: The SD rats were randomly divided into control group，model group and Rg1 treatment group，with 6 rats in each group. The abdominal cavity of the rats in control group was closed after laparotomy；the rats in model group were retrogradely injected with 5% sodium taurocholate (0. 15 μL·kg－1） into the biliopancreatic duct to induce SAP after laparotomy；the rats in Rg1 treatment group were injected with Rg1 (4 mg·kg－1）via the tail vein 30 min before operation of preparing the SAP model；the rats in control group and model group were injected with normal saline 30 min before operation. Enzyme linked immunosorbent assay(ELISA）method was used to detect the levels of serum tumor necrosis factor-α(TNF-α），endotoxin， endothelin 1(ET-1），interleukin-1β(IL-1β）and the activities of serum creatine kinase-MB(CK-MB）， cardiac troponin I(cTnI） and mylase of rats in various groups. Ultrasound imaging system was used to detect the heart rate(HR），left ventricular end-systolic diameter(LVDs）and left ventricular end-diastolic diameter(LVDd）of rats in various groups and calculate the fractional shortening(FS）. Western blotting method was used to detect the expression levels of NADPH oxidase(NOX）2 and NOX4，phosphorylated p38(p-p38），phosphorylated extracellular regulated protein kinase 1/2( p-ERK1/2） and phosphorylated c-Jun N-terminal kinase(p-JNK）proteins in myocardium tissue of rats in various groups. Results: Compared with control group，the levels of TNF- α，endotoxin，IL-1β and ET-1 in serum of the rats in model group were significantly increased (P<0. 05）；the activities of CK-MB，cTnI，and amylase were significantly increased(P<0. 05）. Compared with model group，the levels of TNF- α，endotoxin，IL-1β and ET-1 in serum of the rats in Rg1 treatment group were decreased(P<0. 05），and the activities of CK-MB，cTnI， and amylase were decreased(P<0. 05）. Compared with control group，the HR and LVDs of the rats in model group were significantly increased(P<0. 05），the LVDd had no significant difference(P>0. 05）， and the FS was significantly decreased(P<0. 05）；compared with model group，the LVDs of the rats in Rg1 treatment group were significantly decreased(P<0. 05），the LVDd had no significant difference(P> 0. 05），and the FS was significantly increased (P<0. 05）. The Western blotting results showed that compared with control group ，the expression levels of NOX2 ，NOX4 ，p-p38，p-ERK1/2 and p-JNK proteins in myocardium tissue of the rats in model group were significantly increased (P<0. 05 or P< 0. 01）；compared with model group，the expression levels of NOX2 ，NOX4 ，p-p38 ， p-ERK1/2 and p-JNK proteins in myocardium tissue of the rats in Rg1 treatment group were significantly decreased(P< 0. 05）. Conclusion: Rg1 has a protective effect on cardiac injury in the SAP rats，and its mechanism may be related to reducing myocardial tissue oxidative stress by inhibiring MAPK signaling pathway. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of scutellarin （SCU） on the expression of NOX （NOX2, NOX4） and the degree of liver fibrosis induced by high fat and high sugar in non-alcoholic fatty liver disease （NAFLD）. Methods Sixty rats were randomly divided into normal group, model group, SCU-25 lower dose treatment group［25 mg/（kg·d）, SCU-50 dose in the treatment group［50 mg/（kg·d）］, SCU-100 high dose treatment group ［100 mg/（kg·d） and curcumin positive drug treatment group［200 mg/（kg·d）］, 10 in each group. The normal group was fed with ordinary diet for 24+8 weeks, and the other groups were fed with high-fat and high- sugar diet for 24 weeks to establish NAFLD animal model, and then given Different concentrations of SCU and curcumin intragastric treatment for 8 weeks. After the treatment, the weight of the rats was measured, and the serum samples and liver tissues of the rats were collected under anesthesia. The weight of theliver was measured and the liver index was calculated. ROS content in serum and tissues was detected by ELISA. Using oil red "O" Dyeing, detection of liver lipid deposition and Masson staining to detect the degree of fibrosis of liver tissue; Western blot and immunohistochemistry were used to detect the expression of NOX2 and NOX4 proteins in liver tissues. Results Body weight, liver weight and liver index increased in model group （ P < 0.01）, body weight, liver weight and liver index decreased after different doses of SCU and curcumin treatment group, while body weight and liver weight were significantly decreased in SCU-100 high-dose treatment group and curcumin positive drug treatment group （ P < 0.01）. ROS content in serum and liver tissues of model group was significantly increased （ P < 0.01）, and ROS content was decreased after treatment with different doses of SCU and curcumin （ P < 0.05）. In the liver tissue, the model group showed a large amount of lipid deposition and tissue fibrosis. After treatment with different doses of SCU and curcumin, the lipid deposition was reduced and the degree of liver fibrosis wasimproved. In liver tissue cells, the protein expressions of NOX2 and NOX4 were up-regulated in the model group （ P < 0.05）, but down-regulated in differentdoses of SCU and curcumin （ P < 0.05）, but not dose-dependent. Conclusion SCU may reduce ROS production by inhibiting the expression of NOX2 and NOX4 proteins in liver, thus alleviating the degree of liver fibrosis in NAFLD. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of uremic toxin p-cresol (PC) on the oxidative stress of human coronary artery endothelial cells (HCAECs). Methods HCAECs were cultured in vitro, and treated with different concentrations of free PC alone or combined with 4% albumin for 24 and 48 h, respectively. Cell proliferation was detected by MTT assay; The production of cellular reactive oxygen free radicals (reactive oxygen species, ROS) was detected with specific ELISA kit; The mRNA levels of NADPH oxidases NOX2 and NOX4 were measured with real-time PCR; The protein levels of NOX2, NOX4, p-p38 and p-38 were tested with Western blotting. Results Free and protein-bound PC significantly inhibited the proliferation of HCAECs (P < 0.05), increased the production of ROS (P < 0.05), enhanced the mRNA expression levels of NOX2 and NOX4 (P < 0.05), and up-regulated the protein levels of NOX2, NOX4 and p-p38 in HCAECs (P < 0.05). Conclusion The free and protein-bound PC induces oxidative stress and inhibits the proliferation of HCAECs by regulating the MAPKs signaling pathway

Objective To investigate the protective effect of rosmarinic acid (RA) on hypertensive nephropathy in mice and its underlying mechanism. Methods Thirty male C57BL/6 mice (6~8 weeks) were randomly divided into 3 groups: control group, AngⅡ group (Angiotensin II, 1.46 mg·kg-1·d-1) and AngⅡ+RA group (AngiotensinⅡ1.46 ·kg-1·d-1 + RA50 mg·kg-1·d-1), with 10 mice in each group, and were intervened for 4 weeks. Blood pressure, urinary microalbumin, serum creatinine and blood urea nitrogen were detected. Immunofluorescence assay and Masson staining were performed respectively to observe the macrophage infiltration and the severity of renal fibrosis. In addition, the activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase was determined using NADP+/NADPH test kit; and the level of reactive oxygen species (ROS) in renal tissue was tested by dihydroethidium (DHE) staining. Finally, the expression levels of NADPH oxidase subunits (p22phox, p47phox) and the following proteins were detected by RT-qPCR and western blotting: nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), apoptosis-associated speck-like protein (ASC), Caspase-1, IL-1β and IL-18. Results As compared with the control group, the indicators of blood pressure, urinary microalbumin, serum creatinine and blood urea nitrogen, as well as inflammatory reaction and fibrosis severity of kidney were all significantly increased in AngⅡgroup (P < 0.05). However, RA treatment significantly reversed all the above changes (P < 0.05). Meanwhile, RA also decreased the expression of NADPH oxidase subunits (p22phox and p47phox) and the activity of NADPH oxidase(P < 0.05). The level of ROS in renal tissue and the expression of NLRP3, ASC, Caspase-1, IL-1β and IL-18 were all reduced as well in AngⅡ+RA group. Conclusion RA may play a protective role in hypertensive nephropathy by inhibiting the activation of NADPH oxidase/ROS/NLRP3 inflammasome pathway.

Objective: To investigate the mechanism of DEXmedetomidine alleviating the toxicity and cognitive impairment of oxidative stress mouse model neurons by inhibiting NADPH oxidase 2. Methods: 10 wild-type and 20 Sod1KO male BALB/c mice, 12 months old, according to the purpose of the experiment, they were divided into 3 groups: control group (wild-type mice), model group (oxidative stress mouse model) and DEX group (oxidative stress mouse model + 50 μg/kg DEX treatment), each with 10 mice. The MWM test was used to test the spatial learning and memory abilities of mice. The number of Neu-N+ cells in the hippocampus and the expression level of PSD-95 were detected by immunostaining. The expression levels of Neu-N, PSD-95, TH, total α-synuclein and Ser129-phosphorylated α-synuclein in the hippocampus were detected by Western blot. ROS, MDA and SOD detection kits were used to detect ROS, MDA and SOD levels respectively. The NOX2 level was detected by ELISA kit. The levels of IL-1β, IL-6 and TNF-α were detected by RT-qPCR. Results: The control mice showed normal spatial learning function. Compared with the control mice, the escape latency and swimming distance of the model group increased (P<0.05), while DEX treatment could reduce the escape latency and swimming distance of the model group. Distance (P<0.05). There was no statistical difference in the average swimming speed of the three groups of mice (P>0.05). Compared with control mice, the number of Neu-N+ cells and PSD-95 expression in the hippocampus of the model group decreased (P<0.05), while DEX treatment can increase the number of Neu-N+ cells and PSD in the hippocampus of mice -95 expression level (P<0.05). Compared with the control mice, the expression levels of Neu-N, PSD-95 and TH protein in the hippocampus of the model group mice decreased (P<0.05), and the total α-synuclein and Ser129-phosphorylated α-synonym The expression level of nucleoprotein increased (P<0.05), and DEX treatment can increase the expression level of Neu-N, PSD-95 and TH protein in the hippocampus of mice (P<0.05), and reduce the total α-synuclein and Ser129 -Phosphorylated α-synuclein expression level (P<0.05). Compared with mice in the control group, the level of ROS and MDA in the model group increased, and the level of SOD decreased (P<0.05), while DEX treatment could reduce the level of ROS and MDA, and increase the level of SOD (P<0.05). Compared with the control group, the NOX2 level of the model group increased (P<0.05), and DEX treatment can reduce the NOX2 level (P<0.05). Compared with the control group, the level of IL-1β, IL-6 and TNF-α in the model group increased (P<0.05), and DEX treatment can reduce IL-1β, IL-6 and TNF-α level (P<0.05). Conclusion: The inhibition of NOX2 by DEX can block learning and memory impairment and hippocampal neurodegeneration by inhibiting oxidative stress and neuroinflammation in the mouse model. [ABSTRACT FROM AUTHOR]

Copyright of Mycosystema is the property of Mycosystema Editorial Board and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To observe whether serotonin (5-HT)-mediated proliferation of pulmonary artery smooth muscle cells (PASMCs) is related to the increase of intracellular reactive oxygen species (ROS), and identify the role of NADPH oxidase (NOX) in the production of ROS and 5-HT-mediated proliferation. Methods Tissue block culture method was used to establish a cell line of human PASMCs. Then the cells were divided into 6 groups, normal control (no treatment), 5-HT treatment (1 μmol/L 5-HT), and 3 intervention groups. Then NOX activity was analyzed by using spectrophotometer to calculate the amount of NADPH consumed. ROS production was measured by DCF-DA assay. The expression of phosphorylated-ERK1/2 (p-ERK1/2) was detected by Western blotting. The changes of PASMC proliferation were determined 3H-TdR incorporation assay. Results 5-HT stimulation for 30 min obviously enhanced the NOX activity, ROS production, DNA synthesis, and expression of p-ERK1/2 (all P < 0.05). While the pretreatment of DPI, Tempol or PD98059 could significantly reverse the ERK1/2 phosphorylation and DNA synthesis induced by 5-HT stimulation (both P < 0.05). What's more, DPI also notably reduced the generation of ROS (P < 0.05). Conclusion NOX/ROS may be the key proteins in the signaling pathways of 5-HT mediated proliferation of PASMCs.

Objective: To study Curative efficacy of Observation on the effect of roxathat on renal anemia and its effect on Transferrin saturation (TSAT), cystatin C (Cys C) and NADPH oxidase 2 (NOX2). Methods: 125 patients with renal anemia treated in our hospital from December 2019 to December 2020 were selected and divided into experimental group (n=63) and control group (n=62) by random number table method. The control group was treated with recombinant human erythropoietin and the experimental group was treated with roxathat. Clinical efficacy, TSAT, Cys C, NOX2, erythrocyte count(RBC), hemoglobin (Hb), hematocrit (HCT), ferritin (SF), transferrin (TRF) and ferritin (HEPC) levels and the incidence of adverse drug reactions were compared between the two groups. Results: After treatment, the total effective rate between the two groups was significantly different (P<0.05). Before treatment, there were no significant differences in serum TSAT, Cys C and NOX2 between the experimental group and the control group. After treatment, serum TSAT in experimental group and control group increased over time, and Cys C and Nox2 in experimental group increased and decreased over time, and the difference was significant (P<0.05). Before treatment, there were no significant differences in RBC, HB and HCT test results between the experimental group and the control group. After treatment, RBC, Hb and Hct in experimental group and control group increased with the passage of time, and the difference in experimental group was significant (P<0.05). Before treatment, there were no significant differences in SF, TRF and HEPC test results between the experimental group and the control group. After treatment, serum SF and TRF of both experimental group and control group increased with time, and the experimental group was higher than the control group, and the HEPC decreased with time, and the experimental group was lower than the control group, the difference was significant (P<0.05). The total incidence of ADR in the two groups was 4.76% and 8.06%(P>0.05), respectively. Conclusions: The application of roxathat in patients with renal anemia has a significant effect, which may be related to the effective improvement of serum TSAT, Cys C and NOX2 levels without increasing adverse reactions. [ABSTRACT FROM AUTHOR]

Objective To study the protective effect and its related mechanism of ethanol extract of Chinese propolis (EECP) on kidney of type 1 diabetic rats. Methods Sixty-eight male SD rats were injected intraperitoneally (IP) with streptozotocin (STZ) once at a dose of 55 mg/kg for type 1 diabetic rat model. After 72 hours, the tail vein blood glucose of rat was detected, and rats with blood glucose ＞ 16.7 mmol/L were used as diabetes models. After the model induction, the type 1 diabetic rats were divided into five groups according to random number table method: model group, 50 mg/kg, 100 mg/kg, 200 mg/kg of EECP groups and metformin (75 mg/kg) group, 10 rats for each group. Another 10 normal rats were taken as the normal group. After 12 weeks, blood glucose, creatinine (Scr), urea nitrogen (BUN), malondialdehyde (MDA) and superoxide dismutase (SOD) were measured in each group. HE staining was used to observe renal pathological changes. The protein expressions of NADPH oxidase 4 (NOX4) and p-p38 MAPK were detected by immunohistochemistry and Western blot assay. Results Compared with the normal group, the blood glucose, Scr, BUN, MDA and the expressions of NOX4 and pp38 MAPK were increased significantly in the model group, while the SOD activity decreased significantly (P＜0.05). Compared with the EECP 50 mg/kg group, the blood glucose, Scr, BUN, MDA, and expressions of NOX4 and p-p38 MAPK were significantly decreased in the EECP 100 mg/kg group, EECP 200 mg/kg group and the metformin group, and the SOD activity was significantly increased (P＜0.05). Compared with the EECP 100 mg/kg group and the EECP 200 mg/kg group, the blood glucose, Scr, BUN, MDA and expressions of NOX4 and p-p38 MAPK were significantly reduced in the metformin group, and SOD activity was significantly increased (P＜0.05). Conclusion EECP can improve the renal injury of diabetic rats by reducing blood glucose and enhancing antioxidative ability, and the mechanism may be realized by inhibiting p38 MAPK/NOX4 signal pathway. [ABSTRACT FROM AUTHOR]

The prevalence of obesity and related diseases has increased dramatically in the last decades. Thus, it is of great importance to elucidate the mechanism underlying the formation of adipose tissue. The dynamics of adipose are mainly controlled by adipocyte differentiation, adipocyte enlargement and lipolysis. Adipocyte differentiation is a complex and programmed process in which new adipocytes are derived from multipotent stem cells or preadipocyte precursors. Briefly, adipocyte differentiation is divided into four steps, including initial growth arrest, mitotic clonal expansion, early differentiation, and terminal differentiation-development of mature adipocyte phenotype. Numerous studies have suggested that reactive oxygen species (ROS) could regulate the process of adipocyte differentiation, and thus affect the development of obesity and related diseases. Acting as a kind of highly-active molecule, the main sources of ROS in a cell include mitochondria, NADPH oxidase, xanthine oxidoreductase, xanthine oxidase and nitric oxide synthase. Based on literature in the last years, we reviewed and discussed the role and mechanism of ROS and ROS-generating enzymes in the regulation of adipocyte differentiation, in order to clarify redox-mediated mechanism of adipocyte differentiation and obesity and to provide new clues for the treatment of obesity and related diseases. [ABSTRACT FROM AUTHOR]

Objective: To determine whether NADPH oxidase II(NOX2) is associated in berberine(BBR)-induced protection on HT22 neuronal cells exposed to β amyloid(Aβ). Methods: HT22 neuronal cells were divided into five groups, including the normal cultured Control group, 10 μM Aβ exposure group(Aβ), 1 μM BBR plus 10 μM Aβ treatment group(BBR+Aβ), NOX2-siRNA treatment group(NOX2-siRNA+BBR+Aβ) and scrambled(SC)-si RNA group(SC-si RNA+BBR+Aβ), after an incubation for 24 h, methylthiazolyldiphenyl-tetrazolium(MTT) was used to assess cell viability, lactic dehydrogenase(LDH) reagent kit was used to evaluate the LDH release in the medium, Western blot was taken to evaluate the apoptosis-associated protein Cleaved caspase-3 and NOX2 expressions, reactive oxygen species(ROS) and malondialdehyde(MDA) reagent kits were used to assess the intracellular ROS and MDA levels respectively. Results: Compared with the control group, 10 μM Aβ reduced the viability of HT22 cells, increased LDH activity, intracellular ROS and MDA levels, upregulated cleaved caspase-3 and NOX2 expressions(P<0.05), and 1 μM BBR treatment significantly inhibited the Aβ-induced injury and oxidative effects mentioned above(P<0.05). However, NOX2-siRNA treatment obviously abrogated BBR-induced neuroprotection and anti-oxidative effects(P<0.05), and SC-si RNA showed no significant effect on BBR-mediated neuroprotective effects(P>0.05). Conclusion: NOX2 may mediate BBR-induced neuroprotective effects on the HT22 neuronal cells exposed to Aβ. [ABSTRACT FROM AUTHOR]

Objective This paper aims to investigate the distribution of genotypes and alleles of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase p22phox -930A/G, 242C/T and -675A/T, so as to evaluate the association between three single-nucleotide polymorphisms (SNPs) and risk of atherosclerotic ischemic stroke in permanent resident population of Han nationality living in Shanghai area. Methods The genotypes and allele frequencies of NADPH oxidase p22phox subunit -930A/G, 242C/T and -675A/T were detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis in 205 patients with ischemic stroke and 136 healthy controls. Results In patients with ischemic stroke, the results of PCR-RFLP in variant genetic loci were different. For -930A/G, one band appeared at 268 bp of genotype AA; 2 bands appeared at 197 and 71 bp of genotype GG; 3 bands appeared at 268, 197 and 71 bp of genotype AG. For 242C/T, one band appeared at 348 bp of genotype CC; 2 bands appeared at 188 and 160 bp of genotype TT; 3 bands appeared at 348, 188 and 160 bp of genotype CT. For -675A/T, 2 bands appeared at 158 and 54 bp of genotype TT; 3 bands appeared at 212, 158 and 54 bp of genotype AT. The genotypes and allele frequency of all three SNPs of NADPH oxidase p22phox gene had no significant difference between ischemic stroke patients and healthy controls (P > 0.05). Conclusions The genetic polymorphism of NADPH oxidase p22phox gene -930A/G, 242C/T and -675A/T might have no association with ischemic stroke. DOI: 10.3969/j.issn.1672-6731.2015.09.011

Ischemia reperfusion injury is a common complication of diseases or surgeries such as myocardial infarction, organ transplantation and stroke. It is a leading cause of death of critical patients while satisfying treatments still remains to be developed. During ischemia and reperfusion, neutrophils release a large amount of reactive oxygen species (ROS) to contribute to oxidative stress and recruit more neutrophils to ischemic tissue which expands the inflammatory response and results in tissue injury. Research progresses published in foreign journals on the connection between neutrophil Nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase and tissue ischemia reperfusion injury have been reviewed in this review, so as to provide evidences for the prevention and treatment of major diseases such as cardiovascular and cerebrovascular diseases. [ABSTRACT FROM AUTHOR]

Copyright of Practical Pharmacy & Clinical Remedies is the property of Editorial Department of Practical Pharmacy & Clinical Remedies and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the reaction mechanism of 20-HKTK for aggravating isolated rat myocardial ischemia reperfusion injury (MIKI), i.e., its influence on the active oxygen speejece (KOS ) production and NADPH. Methods Seventy-eight male Wistar rats were randomly divided into the normal control group)Con group) .ischemia-reperfusion model group (IK group), IK+different doses of 20-HKTK groups (10,30.50 nmol/L) and IK+20-HKTK<50 nmol/L)+apocynin(APO) group, 13 cases in each group. The isolated rat heart MIKI model was established. Corresponding dose of 20-HKTK was added into the perfusion solution before ischemia. The myocardial ischemic hemodynamic indexes Here realtimely monitored by the Fowerlab/ 8sp physiological grapher;the myocardial infarction area was measured by the TTC method;the DHK fluorescent probe method was used to detect myocardial tissue fluorescence intensity for expressing the KOS level. The phosphorylation level of p47phox as subunit of NADPH oxidase was detected by the Western blotting; the cytochrome C reduction was used to detect peroxide generated product quantity for expressing the KOS level. Results 20-HKTK dose-dependently aggravated ischemia reperfusion (IK )-in-duced myocardial injury. Compared with the IK group, the myocardial hemodynamic indexes in the IR+ different doses of 20-HKTK groups were significantly decreased, while the myocardial infarction area was significantly increased, the KOS production was further increased, the differences were statistically significant (P<0.01 or P<0.05). After adding APO as an inhibitor of NADPH oxidase. KOS was significantly decreased .which showed the statistical difference compared with the lK+20-HKTK(50 nmol/L) group(P<0.05). Compared with the IK group.the cardiac phosphorylation level of p47phox subunit and NADPH oxidase activity in the lK+20-HKTK(50 nmol/L)+APO group were significantly increased, the differences were statistically significant)(P<0.05). Conclusion 20-HKIK aggravate MIKI by activating NADPH oxidase to induce excessive KOS production. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of liraglutide on renal function, the glomerular morphology in electron microscope and oxidase subunit of dihydronicotinamide adenine dinuclectide phosphate(NADPH)--P22phox and P47phox in kidney in rats with insulin resistance(IR). Methods Fifty-four male Wistar rats were divided into normal diet group(group A, n=16) and high-fat diet group(n=38). Hyperinsulinemic-euglycemic clamp test was performed at the waking state after 8 weeks feeding. Glucose infusion rate(GIR) was measured to determine if IR rats model was successful. The rats with high-fat diet were randomly divided into three groups:high-fat diet group(group B, n=11), liraglutide 100μg/(kg · d) group (group C, n=11), liraglutide 200μg/(kg·d) group(group D, n=11). The rats with normal diet was group A(n=11). Daily subcutaneous injections of saline were given group A, B,while liraglutide intervention was given in group C,D. After 2 weeks, biochemical markers were measured in each group. Realtime Quantitative PCR and Western blotting were used for detecting the expression of P22phox and P47phox in kidney. Renal ultrastructure was observed by transmission electron microscope. LSD t test was performed in comparison between the two groups, while one way variance analysis for multiple groups comparison. Results (1) Compared with group A, the expression of P22phox and P47phoxin were significantly increased in group B (P22phox mRNA:4.9±0.4 vs 1.0±0,P22phox protein:2.72±0.20 vs 1.27±0.24;P47phox mRNA:4.8±0.8 vs 1.0 ± 0,P47phox protein: 2.17 ± 0.39 vs 1.13 ± 0.15,t=4.225-16.041, all P<0.05). (2) Compared with the group B, the expression level of P22phox and P47phox were decreased in liraglutide groups (P22phox mRNA: 2.3 ± 0.4, 4.5 ± 0.4, 4.9 ± 0.4 in group D,C,B, respectively; P22phox protein 1.75 ± 0.13, 2.32 ± 0.21, 2.72 ± 0.20;P47phox mRNA: 2.2 ± 0.3, 3.6 ± 0.4, 4.8 ± 0.8,in group D, C, B, respectively; P47phox protein:1.30±0.18, 1.66±0.15, 2.17±0.39), and group D decreased more significantly than group C (t=6.482, 3.401, 4.875, 2.067, all P<0.05). (3) The basement membrane of glomerular in group B was uneven thickness, with part of the podocytes swelling, or even disappear. It was improved after the intervention of liraglutide, especially in group D. Conclusion Reducing oxidative stress by inhibiting the expression of P22phox, P47phox in kidney, maybe one of the kidney protection mechanisms of liraglutide on IR rats. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Agro-Environment Science is the property of Journal of Agro-Environment Science Editorial Board and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate effects of PKC/NADPH oxidase on reactive oxygen species (ROS) in Human umbilical vein endothelial cells (HUVECs) cultured with high glucose. Methods: The experiments were divided into six groups, including control group, NaOH control group, DMSO control group, group treated with glucose (20 mM) for 4 hours (high-glucose group), group which was pretreated phorbol ester (1 mol) for half an hour then was stimulated by glucose (20 mM) for 4 hours (phorbol ester group) and group which was pretreated hypericin (4 mol) for half an hour then was stimulated by glucose (20 mM) for 4 hours (hypericin group); Human umbilical vein endothelial cells was isolated by type Ⅱ collegease; flow cytometry was used to detect intracellular ROS production; immunofluorescence was used to investigate factor Ⅷ and p47 phox location in HUVECs. Results: ① Compared with control group, intracellular ROS of high-glucose group were significantly increased (P<0.05, n=3), Compared with control group and, high-glucose group, intracellular ROS of phorbol ester group were significantly increased (P<0.05, n=3), Compared with control group and, high-glucose group, intracellular ROS of hypericin group were significantly decreased (P<0.05, n=3); ② p47 phox mostly located cytoplasm for control group and hypericin group, p47 phox mostly located cell membrane for high-glucose group and phorbol ester group. Conclusion: PKC/NADPH oxidase can regulate ROS generation in HUVECs induced with high glucose by translocation of p47 phox. [ABSTRACT FROM AUTHOR]

The effects of wangzaozin A, a kind of ent-kaurane diterpenoids, on the growth, cellular morphology, NBT-reducing ability, cellular uptake and cell surface markers CDllb of HL-60 cells were determined by trypan blue exclusion method, giemsa stainning and flow cytometry. The results showed that 0. 2~0. 8 µmol/L wangzaozin A could inhibit the growth of HL-60 cells, cells treated with 0. 6 and 0.8 µmol/L wangzaozin A presented obviously G1 arrest. With the increase of the concentration of wangzaozin A and the treatment time, metamyelocytes, banded neutrophils and segmented neutrophils increased, nuclear/cytoplasm ratio decreased, granular substance in cells increased; at the same, NBT-reducing ability, cellular uptake and the expression of CD11b of HL-60 cells enhanced remarkedly, with a obvious dose-and time-dependent manner. The results showed that differentiation of human HL-60 cells into granulocyte could be induced by wangzaozin A. Further, the detection by fluorescence probe DCF showed that ROS in cells treated with 0. 6 and 0. 8 µM wangzaozin A after 12 h increased obviously? the expression of CD11b induced by wangzaozin A could be markedly inhibited by antioxidant NAC and APO which is the inhibitor of NADPH oxidas. It indicated that wangzaozin A could induce the differentiation of HL-60 cells by up-regulating concentration of NADPH oxidase-derived reactive oxygen species. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect of treatment with apocynin(one NADPH oxidase inhibitor) against biophenol a(BPA)-induced injury in sperms of male adult mice. Methods: Male adult mice were stimulated with BPA and simultaneously treated with apocynin(1 mg/kg, 10 mg/kg) for 7 days. Testis and serum were collected for biochemical analysis. Results: Exposure to BPA led to reduced number and motility of sperms of epididymises and serum levels of testosterone and luteinizing hormone. Treatment of BPA mice with apocynin enhanced the number and motility of sperms of epididymises, but did not affect the serum levels of testosterone and luteinizing hormone. In addition, exposure to BPA led to enhanced formation of malondialdehyde in testis, and treatment of BPA mice with apocynin reduced formation of malondialdehyde in testis. Conclusion: Apocynin attenuated BPA-induced injury in sperms of male adult mice. [ABSTRACT FROM AUTHOR]

Oxidative damage mediated by the abnormal activation of NADPH oxidase and the resulting excessive ROS generation is the pathogenesis for various diseases. Chinese herbs can play a role in the antioxidant treatment by inhibiting NADPH oxidase, which is meaningful for the treatment of pathological conditions such as injury of tissues, blood vessels and nerves, atherosclerosis, ischemia reperfusion, hypertension and hyperglycemia. In this paper, different forms of Chinese herbs including monomers, compounds and Chinese patent medicines with the inhibitory effect against NADPH oxidase would be reviewed, in order to explain and generalize their possible functions and the target mechanism for inhibition., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Chinese Pharmaceutical Association.)

Objective: To investigate the effect of NADPH oxidase inhibitor apocynin on exercise-induced proteinuria and its related mechanism., Methods: Thirty-two SD rats were randomly divided into the control group (group C), control + drug group (group CA), exhaustive exercise group (group E), exhaustive exercise + drug group (group EA). The rats were administrated apocynin at 10 mg/kg weight,once a day for three days, and one hour after the drug injection, a one-time exhaustive exercise was performed. After exhaustive exercise, urine protein, blood urea nitrogen (BUN), and kidney reactive oxygen species (ROS) concentration, NOS activity, NOS and 3-NT concentration were detected., Results: In comparison to control group urinary protein (UP), ROS, inductible nitric oxide synthase (iNOS), 3-NT levels increased significantly in group E while those in group EA did not change., Conclusions: The elevated renal NADPH oxidase activity by exhaustive exercise induced ROS that can rapidly react with NO, and then produces excess peroxynitrite, which contributes to occurrence of exercise-induced proteinuria.