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Copyright of Journal of China Medical University is the property of Journal of China Medical University Editorial Office 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.)

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.)

Copyright of Bulletin of Botanical Research is the property of Bulletin of Botanical Research 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 effect of Na+/Ca2+ exchanger inhibitors SN-6 and calcium channel blocker verapamil on potassium-stimulated expression of aldosterone synthase in adrenocortical carcinoma cell line NCI-H295R(H295R). Methods H295R cells were treated in different groups, including control group, K+ (15 mmol/L) treated group, verapamil (10 μmol/L) group, SN-6 (10 μmol/L) group, combination of K+/verapamil treated group, combination of K+/SN-6 treated group, combination of K+/verapamil and SN-6 treated group. Real-time PCR was used to detect the mRNA expression of aldosterone synthetase (CYP11B2), and FLIPR Calcium 6 was used to detect the intracellular calcium ion level. Results Compared with the control group, K+ stimulated CYP11B2 mRNA expression. Both SN-6 and verapamil decreased K+ induced CYP11B2 mRNA expression(P＜0.01). Compared with the K++SN-6 treated group, the K+,SN-6 and verapamil treated group all significantly inhibited CYP11B2 mRNA expression (P＜0.001). Both of SN-6 and verapamil significantly reduced the intracellular calcium level stimulated by K+ (P＜0.0001). Conclusions Both SN-6 and verapamil inhibit K+-induced expression of aldosterone synthase in adrenocortical carcinoma H295R cells. The inhibitory effect is more significant when treated by the combination of verapamil and SN6.

Copyright of Basic & Clinical Medicine is the property of Editorial Office of Basic & Clinical Medicine 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.)

Stroke is one of the leading causes of disability and death in China, but its mechanism has not been thoroughly elucidated. As an important class of cells in maintaining neurological homeostasis, the intracellular calcium signaling of glial cells plays a dual role in mitigating and exacerbating neuronal damage in stroke and largely determines the progression and outcome of stroke. In this review of the literature, focusing on astrocytes, which account for the largest proportion of glial cells, we review the mechanism of glial calcium signaling after stroke and its effect on post-stroke neurological function, to provide reference for post-stroke neuroprotection and repair. [ABSTRACT FROM AUTHOR]

BACKGROUND: Disorders of calcium metabolism mediate the occurrence and development of chronic fluorosis, but the specific molecular mechanism has not been elucidated and there is little systematic discussion on the role of calcium ion (Ca2+) in the pathogenesis of chronic fluorosis. OBJECTIVE: To review the role of Ca2+ in chronic fluorosis, thereby providing new ideas and perspectives for the exploration of the molecular mechanism of chronic fluorosis and the development of targeted drugs. METHODS: “Ca2+, fluorosis, pathogenesis, calcium overload, oxidative stress, endoplasmic reticulum stress, mitochondrial damage, apoptosis” were used as Chinese and English keywords, and the relevant literatures included in PubMed database and CNKI database from January 2000 to January 2022 were retrieved. After removal of obsolete, repetitive and low-credibility documents, 110 documents were finally included. RESULTS AND CONCLUSION: Ca2+ plays an important role in the pathogenesis of chronic fluorosis. The calcium paradox forms of low extracellular calcium caused by bone calcium metabolism disorder and of high intracellular calcium caused by intracellular Ca2+ metabolism disorder jointly induce the damage of fluoride to the bone and non-bone tissues. Intracellular Ca2+ metabolism disorder, with calcium overload as the core link, mediates the occurrence and development of chronic fluorosis. The specific process is as follows: fluorine promotes the production of chronic fluorosis through the inhibition of calcium transporters/enzymes in the plasma membrane and endoplasmic reticulum and the interference of gene expression levels. Cytoplasmic calcium is overloaded, thereby activating the downstream calcium signal transduction pathway, forming a unified negative regulatory network with multiple mechanisms, such as oxidative stress, endoplasmic reticulum stress, mitochondrial damage, and jointly inducing apoptosis in bone and soft tissue cells. In contrast, calcium agents and inhibitors that act on intracellular calcium-related targets (LTCC Cav1.2, NMDARs, and CaM-CAMKII) exert therapeutic effects by reversing fluoride-induced calcium paradoxes. Recovery from Ca2+ metabolism disorders is an important approach for treating chronic fluorosis. From another point of view, this not only provides an immediate theoretical basis for the current clinical application of calcium agents, but also provides new ideas and confidence for the development of drugs acting on calcium-related targets in the future. [ABSTRACT FROM AUTHOR]

Copyright of South China Fisheries Science is the property of South China Fisheries 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.)

Copyright of Bulletin of Botanical Research is the property of Bulletin of Botanical Research 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.)

Copyright of Modern Food Science & Technology is the property of Editorial Office of Modern Food Science & Technology 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.)

Copyright of West China Journal of Stomatology is the property of Sichuan University, West China College of Stomatology 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.)

Copyright of Acta Edulis Fungi is the property of Acta Edulis Fungi 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.)

Copyright of Acta Edulis Fungi is the property of Acta Edulis Fungi 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 method for culturing cortical neurons from neonatal SD rats. Methods: The cerebral cortex of 24-hour-old SD rats were isolated and centrifuged before trypsin digestion. The cell suspension obtained after trypsin digestion was planted into L-polylysine coated culture dish or confocal dish. The primary culture of neurons was carried out in a culture medium contained B27 and Neurobasal-A. The growth of cultured cells was checked under inverted microscope. Immunofluorescence histochemistry was used to identify the purity of neurons by using microtubule-associated protein 2（MAP-2） as a marker of neurons. The changes of intracellular calcium signal after electrical stimulation was observed in Fluo4-AM loaded primary neurons to verify the physiological state of neurons. Results: The neurons cultured with this method were closely adherent, evenly dispersed and in good condition. The neurites of the neurons were interconnected to form a network. MAP-2 immunofluorescence histochemistry showed that the purity of neurons was more than 95%. The stimulation-induced intracellular calcium signal indicated that the cultured neurons had good biological function. Conclusions: This method can make primary cultured cortical neurons of SD rats with high purity and good biological function. [ABSTRACT FROM AUTHOR]

BACKGROUND: Previous studies have mostly focused on immune factors involved in the pathogenesis of rheumatoid arthritis. Recently, increasing attention has been paid to the role of biomechanical factors in the occurrence and development of rheumatoid arthritis. OBJECTIVE: To explore the mechanism by which Piezo1 mediates apoptosis of fibroblast-like synovial cells in rheumatoid arthritis through MAPK/ERK5 signaling pathway. METHODS: The tissue block method was used to culture synovial cells of rheumatoid arthritis. The stretch stress model of cells in vitro was constructed by Flexcell 5000T cell stretch stress system, and piezo1 siRNA gene interference vector and overexpression plasmid were constructed. According to the preliminary experimental results and treatment plan, fibroblast-like synovial cells of rheumatoid arthritis were divided into six groups: siRNA interference group, overexpression plasmid group, blank control group, siRNA interference+BIX02188 group, overexpression plasmid+BIX02188 group, and blank control+BIX02188 group. The expression of Piezo1, ERK5 and apoptosis-associated genes were detected by RT-PCR, the intracellular calcium content was detected by Fluo-3 AM probe, and the apoptotic level was detected by AV-PI kit. RESULTS AND CONCLUSION: The intracellular Ca2+ content of the siRNA interference+BIX02188 group was significantly lower than that of the siRNA interference group (P < 0.05); the intracellular Ca2+content of the overexpression plasmid+BIX02188 group was significantly lower than that of the overexpression plasmid group (P < 0.05). The relative expression of Piezo1 and ERK5 mRNA in the siRNA interference group was significantly lower than that in the blank control group (P < 0.05), and that in the overexpression plasmid group was significantly higher than that in the blank control group (P < 0.05). The expression of Piezo1 mRNA did not change after BIX02188 inhibition; however, the relative expression of ERK5 mRNA in the siRNA interference+BIX02188 group was significantly lower than that in the siRNA interference group (P < 0.05), and the expression of ERK5 mRNA in the overexpression plasmid+BIX02188 group was significantly lower than that in the overexpression plasmid group (P < 0.05). The early apoptotic rate, the late apoptotic rate and the total apoptotic rate in the siRNA interference group were significantly lower than those in the blank control group (P < 0.05), whereas the early apoptotic rate, the late apoptotic rate and the total apoptotic rate in the overexpression plasmid group were significantly higher than those in the blank control group (P < 0.05). To conclude, the overexpression of Piezo 1 protein can promote the apoptosis of rheumatoid arthritis fibroblast-like synovial cells, and the apoptotic signal mediated by the MAPK/ERK5 signaling pathway can act as the potential target gene for treating rheumatoid arthritis. [ABSTRACT FROM AUTHOR]

Objective To explore the effect of dopamine reuptake inhibition on sperm motility in mice and humans and its mechanism of action. Methods After the sperm were treated with dopamine reuptake inhibitors GBR 12909 and GBR 12935, the computer-assisted semen analysis system (Computer-Assisted Semen Analysis, CASA) assess sperm motility; eosin-nigrosine staining to detect sperm viability; detect intracellular pH (pHi) and intracellular calcium (Intracellular Calcium, [Ca2+]i) level changes by fluorescent probes; protein Western blotting was used to detect changes in protein phosphorylation; Coomassie Brilliant Blue G250 staining to detect changes in acrosome reaction. Results GBR 12909 and GBR 12935 can significantly inhibit sperm motility in mice and humans without affecting sperm survival, and make sperm cells (Ca2+)i decreases, pHi increases, glycogen synthase kinase 3 alpha (Glycogen Synthase Kinase 3 Alpha, GSK3α) phosphorylation and protein kinase A (Protein Ki-nase A, PKA) substrate phosphorylation levels decrease. Among them, GBR 12909 can promote Sperm capacitation-related protein tyrosine phosphorylation is not observed in GBR 12935; neither affects the incidence of acrosome reaction induced by A23187 after sperm capacitation in mice. Conclusion Dopamine reuptake inhibitors GBR 12909 and GBR 12909 GBR 12935 can reduce sperm [Ca2+]i, increase pHi, and may reduce sperm motility by down-regulating GSK3α phosphorylation and PKA substrate phosphorylation. [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.)

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 changes in myocardial calcium currents in rats subjected to forced running exercise during acute hypoxia and their association with myocardial injury., Methods: Forty SD rats were randomized into quiescent group and running group either in normal oxygen (NQ and NR groups, respectively) or in acute hypoxia (HQ and HR groups, respectively). Hypoxia was induced by keeping the rats in a hypobaric oxygen chamber (PaO 2 =61.6kpa) for 4 h a day; the rats in the two running groups were forced to run on running wheels for 4 h each day. Rat ventricular myocytes was isolated by enzymatic digestion for recording action potentials and currents using patch clamp technique, and confocal Ca 2+ imaging was used to monitor intracellular Ca 2+ levels. The expressions of Cav1.2 channel and the cardiac ryanodine receptor (RyR2) were determined using Western blotting., Results: Compared with those in NQ group, the rats in HR group showed significantly decreased SOD activity ( P < 0.01), increased h-FABP, hs-CRP and IMA levels ( P < 0.05 or 0.01), obvious myocardial pathology, and prolonged APD50 and APD90 ( P < 0.05). Of the different stress conditions, forced running in acute hypoxia resulted in the most prominent increase of the densities of ICa, L currents, causing also a significant left shift of the steady state activation curve and a significant right shift of the steady state inactivation curve. Compared with those in NQ group, the rats in NR, HQ and HR groups all exhibited higher rates of spontaneous calcium wave events in the cardiac myocytes, increased frequency of calcium sparks with lowered amplitude, enhanced calcium release amplitude in the ventricular myocytes, and delayed calcium ion reabsorption; in particular, these changes were the most conspicuous in HR group ( P < 0.05 or 0.01). There was also a significant increase in the protein levels of Cav1.2 channel and RyR2 receptor in HR group ( P < 0.05 or 0.01)., Conclusions: The mechanism of myocardial injury in rats subjected to forced running in acute hypoxia may involve the increase of oxidative stress and calcium current and intracellular calcium overload.

It has been shown that ischemia preconditioning (IPC) can attenuate the myocardial injury induced by ischemic and reperfusion. But it was rarely used in clinic due to its inoperability. Previous studies indicate that electroacupuncture (EA) pretreatment can mimic myocardial ischemia preconditioning (MIPC) to produce cardioprotective effect. The activated adenosine A 2 b receptor has been proven to be involved in mediating the cardioprotection of IPC. In the studies on acupuncture analgesia, it was reported that adenosine receptor was activated by acupuncture stimulation, and acupuncture pretreatment can affect the acti-vities of intracellular A 2 b receptor. Based on those mentioned above, it is highly likely that the A 2 b receptor may also participate in the cardioprotection produced by acupuncture pretreatment. In this paper, we comprehensively reviewed relevant studies regarding 1) the cardioprotective effect of IPC and its limitations, 2) the similar cardioprotection produced by both acupuncture pre-treatment and IPC, 3) the mechanism underlying myocardial ischemic injury and intracellular calcium regulation, 4) the acti-vation of adenosine receptors and effects of acupuncture, 5) the relationship between adenosine receptors and intracellular calcium ion, and 6) the effect of acupuncture on adenosine receptors, so as to provide a novel assumption that A 2 b receptor may be a key factor in mediating the cardioprotection of acupuncture pretreatment. Our future research will systematically explore the me-chanism of acupuncture pretreatment in protecting ischemic myocardium from myocardial cell adenosine A 2 b receptor and intracellular calcium signal transduction related factors.

The hawthorn leaves have the effect of activating blood, removing blood stasis, regulating qi through the veins, dissolving turbidity and lowering lipid. Procyanidinis is one of its main active components and plays an important role in regulating vasoactivity. Previous studies showed that the regulating effect of procyanidins was related to its regulation on nitric oxide secretion from vascular endothelial cells, and this effect was dependent on the extracellular calcium concentration, suggesting that the changes in intracellular calcium ion concentration in endothelial cells may play a key role in this process. However, the research on this issue is still insufficient so far. This study is aimed to observe the effect of hawthorn leaf oligomeric procyanidins (HLP) on calcium mobilization of vascular endothelial cells, and investigate the underlying mechanism. Human umbilical vein endothelial cells (HUVEC) were cultured in vitro and labeled with Fura-2. HUVEC were treated with HLP at concentrations of 6.25, 12.5, 25 and 50 mg·L⁻¹, and the intracellular calcium concentrations were measured with a living cell microscope for 30 min. HLP increased the intracellular calcium concentration of HUVEC in a concentration dependent manner; and the intracellular calcium concentrations in 25 and 50 mg·L⁻¹ HLP groups were significantly higher than that in the normal group. With the use of calcium-free incubation buffer, addition of calcium chelating agent EGTA in incubation buffer, or use of inhibitors for sodium calcium exchanger, the effect of HLP was significantly inhibited. On the other hand, the effect of HLP could also be weakened by inhibiting the calcium release from the intracellular storage. In conclusion, these results suggest that HLP can elicit calcium mobilization in vascular endothelial cells, which may be one of the mechanisms for its vascular modulatory activity; and this calcium mobilizing effect may be achieved through promoting both extracellular calcium influx and intracellular calcium release, additionally the former may be related to activating the reverse transport of Na⁺-Ca²⁺ exchangers on the cell membrane., 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.)