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Antler velvet polypeptide (VAP) is a prominent bioactive component of antler velvet. Whereas uncharacterized crude extracts have typically been used in pharmacological studies, in this study, the velvet polypeptide was isolated and purified by acid water extraction, ethanol precipitation, ammonium sulfate fractionation and precipitation, and chromatography, progressively. Human umbilical vein endothelial cells (HUVECs) were induced with [H.sub.2][O.sub.2] followed purified polypeptide treatment. Cell viability was evaluated by MTT assay. The apoptosis of cells was detected by fluorescence microscopy and flow cytometry. A cell analyzer was used to measure the mitochondrial membrane potential. The intracellular reactive oxygen species (ROS) levels were determined by flow cytometry. Oxidative stress related biochemical parameters were detected, and the expression of apoptosis-related proteins was examined by Western blot analysis. The results indicated that a 7.0 kDa polypeptide (VAP II) was isolated from antler velvet. VAP II enhanced cell viability, decreased cell apoptosis, reversed depolarization of mitochondrial membrane potential, decreased ROS levels, inhibited oxidative stress, and regulated the downstream signaling apoptotic cascade expression caused by [H.sub.2][O.sub.2]. The protective effects of VAP II on HUVECs suggests a potential strategy for the treatment of cardiovascular disease. Key words: antler velvet polypeptides, oxidative stress, antioxidant, apoptosis. Le polypeptide de bois de velours (VAP pour << antler velvet polypeptide >>) est un important compose bioactif des bois de velours. Alors que des extraits bruts non caracterises ont habituellement ete utilises dans le cadre d'etudes pharmacologiques, dans cette etude, nous avons isole et purifie le polypeptide de velours par une extraction acide-eau, la precipitation dans l'ethanol ainsi que le fractionnement et la precipitation a l'aide de sulfate d'ammonium, avec le passage progressif dans une colonne de chromatographie. Nous avons obtenu des cellules HUVEC (pour << human umbilical vein endothelial cells >>) par une induction l'aide de [H.sub.2][O.sub.2] suivie d'un traitement de purification des polypeptides. Nous avons evalue la viabilite des cellules l'aide du test MTT. Nous avons decele les cellules apoptotiques a l'aide de la microscopie par fluorescence et de la cytometrie en flux. Nous avons utilise un analyseur de cellules pour mesurer le potentiel des membranes mitochondriales. Nous avons mesure les derives reactifs de l'oxygene (ou ROS pour << reactive oxygen species >>) intracellulaires par cytometrie en flux. Nous avons detecte les parametres biochimiques lies au stress oxydatif et etudie l'expression des proteines liees a l'apoptose a l'aide de la technique d'immunobuvardage de Western. Les resultats ont revele l'isolation d'un polypeptide de 7,0 kDa (VAP II) partir de bois de velours. Le VAP II pourrait entrainer une augmentation de la viabilite des cellules, une attenuation de l'apoptose cellulaire, la depolarisation inverse du potentiel des membranes mitochondriales, diminuer les taux de ROS, inhiber le stress oxydatif et assurer la regulation de l'expression de la cascade de la signalisation apoptotique causee par le [H.sub.2][O.sub.2] en aval. Les effets protecteurs du VAP II contre les lesions des cellules HUVEC ont permis d'obtenir une strategie eventuelle dans le traitement de la maladie cardiovasculaire. [Traduit par la Redaction] Mots-cles : polypeptide de bois de velours, stress oxydatif, antioxydant, apoptose., Introduction There has recently been a surge of interest in the benefits from the natural products used in traditional and herbal medicines. To date, the majority of studies conducted worldwide [...]

Microwaves may exert adverse biological effects on the cardiovascular system at the integrated system and cellular levels. However, the mechanism underlying such effects remains poorly understood. Here, we report a previously uncharacterized mechanism through which microwaves damage myocardial cells. Rats were treated with 2450 MHz microwave radiation at 50,100,150, or 200 mW/[cm.sup.2] for 6 min. Microwave treatment significantly enhanced the levels of various enzymes in serum. In addition, it increased the malondialdehyde content while decreasing the levels of antioxidative stress enzymes, activities of enzyme complexes I-IV, and ATP in myocardial tissues. Notably, irradiated myocardial cells exhibited structural damage and underwent apoptosis. Furthermore, Western blot analysis revealed significant changes in expression levels of proteins involved in oxidative stress regulation and apoptotic signaling pathways, indicating that microwave irradiation could induce myocardial cell apoptosis by interfering with oxidative stress and cardiac energy metabolism. Our findings provide useful insights into the mechanism of microwave-induced damage to the cardiovascular system. Key words: microwave radiation, myocardial cell, oxidative stress, energy metabolism. Les micro-ondes pourraient avoir des effets biologiques nefastes sur le systeme cardiovasculaire: dans son integrite comme au niveau cellulaire. Cependant, on connait toujours peu leurs mecanismes sous-jacents. Dans ces travaux, nous rapportons un mecanisme encore jamais caracterise qui mene a des lesions des cellules myocardiques. A cet effet, nous avons administre a des rats des rayonnements de micro-ondes de 2450 MHz a 50,100, 150 ou 200 mW/[cm.sup.2] pendant 6 min, ce qui a entraine une augmentation marquee des taux seriques de divers enzymes. Cette intervention a aussi entraine une augmentation des taux de malondialdehyde ainsi qu'une diminution des taux des enzymes du stress oxydatif, de l'activite des enzymes des complexes I a IV et des taux d'ATP dans le tissu myocardique. Mais surtout, les cellules myocardiques irradiees presentaient des dommages structurels et subissaient l'apoptose. En fait, l'analyse par buvardage de Western a revele la presence de modifications importantes des taux d'expression des proteines jouant un role dans les voies de signalisation de la regulation du stress oxydatif et de l'apoptose, ce qui indique que l'irradiation par les micro-ondes peut induire l'apoptose dans les cellules myocardiques en interferant avec le stress oxydatif et le metabolisme energetique cardiaque. En somme, nos resultats donnent une idee concrete du mecanisme responsable des dommages causes par les micro-ondes au systeme cardiovasculaire. [Traduit par la Redaction] Mots-cles: rayonnement de micro-ondes, cellule myocardique, stress oxydatif, metabolisme energetique., Introduction Microwaves are electromagnetic waves with wavelengths ranging from 1 mm to 1 m and frequencies between 300 MHz and 300 GHz (Gupta 2014; Shahin et al. 2013). Microwave technology [...]

Fibroblast growth factor 21 (FGF-21), which is a modulator of glucose and lipid homeostasis, acts as a novel therapeutic reagent for many metabolic perturbations. However, its potential as a treatment for cardiovascular disease, especially atherosclerosis (AS) has not been fully explored. Here, we report that recombinant FGF-21 improves resistance to cell damage from oxidative stress in vitro, and from atherosclerosis in vivo. Human umbilical vein endothelial cells (HUVECs) were induced with [H.sub.2][O.sub.2], followed by treatment with high purity recombinant FGF-21. The results indicated that FGF-21 significantly enhanced cell viability and decreased the degree of DNA fragmentation in HUVECs, as caused by [H.sub.2][O.sub.2] stress induction. Further studies revealed that FGF-21 inhibited [H.sub.2][O.sub.2]-induced cell apoptosis by preventing the activation of mitogen-activated protein kinase (MAPK) signaling pathways. In an established rat model, FGF-21 dramatically improved the condition of atherosclerotic rats by decreasing serum levels of total triglyceride (TG), low density lipoprotein cholesterol (LDL-C), and total cholesterol (TC), and by increasing the serum levels of high density lipoprotein cholesterol (HDL-C). FGF-21 also has antioxidant effects in the atherosclerotic rat, such that increased levels of superoxide dismutase, reduced glutathione, and reduced malondialdehyde were observed. These data provide novel insight into the potential use of FGF-21 in the prevention and treatment of human cardiovascular diseases. Key words: FGF-21, HUVECs, oxidative stress, apoptosis. Le facteur de croissance fibroblastique 21 (FGF-21), un modulateur de l'homeostasie du glucose et des lipides, agit comme nouvel agent therapeutique de plusieurs troubles metaboliques. Cependant, son potentiel comme traitement de la maladie cardiovasculaire, notamment l'atherosclerose (AS), n'a pas ete pleinement explore. Les auteurs rapportent ici que le FGF-21 recombinant ameliore la resistance au dommage cellulaire cause par le stress oxydant in vitro et l'atherosclerose in vivo. Des cellules endotheliales de la veine de cordon ombilical humain (HUVEC) ont ete traitees au [H.sub.2][O.sub.2], puis au FGF-21 recombinant de haute purete. Les resultats ont indique que le FGF-21 accroissait significativement la viabilite cellulaire et diminuait le degre de fragmentation d'ADN provoquee chez les cellules HUVEC par le stress du au traitement au [H.sub.2][O.sub.2]. Des etudes additionnelles ont revele que le FGF-21 inhibait l'apoptose induite par le [H.sub.2][O.sub.2] en prevenant l'activation de la signalisation par la voie de MAPK. Dans un modele etabli, le FGF-21 ameliorait de facon importante les conditions des rats atteints d'atherosclerose en diminuant les niveaux seriques des triglycerides totaux (TG), de cholesterol lie aux lipoproteines de faible densite (LDL-C), du cholesterol total (TC) et en augmentant le cholesterol lie aux lipoproteines de haute densite (HDL-C). Le FGF-21 exercait aussi un effet antioxydant chez le rat souffrant d'atherosclerose, car des augmentations de SOD et de GSH et une diminution de MDA ont ete observees. Ces donnees donnent un nouvel apercu du potentiel du FGF-21 dans la prevention et le traitement des maladies cardiovasculaires chez l'humain. [Traduit par la Redaction] Mots-cles: FGF-21, HUVEC, stress oxydant, apoptose., Introduction Atherosclerosis (AS) is a chronic and degenerative disease of the large artery walls. It is the single most important cause of cardiovascular disease (CVD), which is a predominant health [...]

New therapeutic approaches are needed to improve the survival rate from pancreatic cancer, one of the most lethal human malignancies. In this study, JF305 cells were treated with microwaves at doses of 2.5, 5.0,10.0,15.0, and 20.0 mW/[cm.sup.2] for 20 min. The inhibition of JF305 cell proliferation was tested using the MTT assay. Apoptotic cells were detected with Hoechst 33258 staining and a Nucleo-Counter NC-3000. The expression of apoptosis-related proteins was examined with Western blot. The results showed that microwaves inhibited the growth of JF305 cells in a dose-dependent manner, and caused morphological changes in apoptotic body formation. The percentages of apoptosis detected using annexin V-fluorescein isothiocyanate (FITC) were 4.0%, 10.0%, 12.0%, and 30.0% with the dosage of microwave (0, 5.0,10.0, and 20.0 mW/[cm.sup.2]), respectively. Treatment with microwaves increased the activity of caspase-9 and caspase-3, down-regulated the expression of Bcl-2, and up-regulated the expression of Bax and CytoC. In addition, the expression level of p65 was increased whereas the level of IκBα down-regulated. Those results suggest that microwaves inhibit cell growth and induce apoptosis in JF305 cells through an NF-κB-regulated mitochondria-mediated pathway. Key words: anticancer, microwave, JF305 cells, apoptosis. De nouvelles approches therapeutiques sont requises afin d'ameliorer le taux de survie des patients atteints du cancer du pancreas, un des cancers les plus letaux chez l'humain. Dans cette etude, les cellules JF305 ont ete traitees par des microondes a des doses de 2,5, 5,0, 10,0, 15,0 et 20,0 mW/[cm.sup.2] pendant 20 minutes. L'inhibition de la proliferation des cellules JF305 a ete testee a l'aide d'un dosage au MTT. Les cellules en apoptose ont ete detectees par une coloration au Hoechst 33258 sur un Nucleo-Counter NC-3000. L'expression de proteines reliees a l'apoptose a ete examinee par buvardage Western. Les resultats ont montre que les microondes peuvent inhiber la croissance des cellules JF305 en fonction de la dose et causer des changements morphologiques dans la formation de corps apoptotiques. Les pourcentages de cellules en apoptose detectes par l'Annexine V-FITC etaient respectivement de 4,0, 10,0, 12,0 et 30,0 % en fonction de la dose de microondes (0, 5,0, 10,0, et 20,0 mW/[cm.sup.2]). Le traitement aux microondes accroissait l'activite de la caspase-9 et de la caspase-3, regulait a la baisse l'expression de Bcl-2 et regulait a la hausse l'expression de Bax et CytoC. En plus, le niveau d'expression de p65 etait accru alors que celui de IκBα etait diminue. Ces resultats suggerent que les microondes inhibent la croissance cellulaire et induisent l'apoptose des cellules JF305 par l'intermediaire d'une voie mitochondriale regulee par NF-κB. [Traduit par la Redaction] Mots-cles: anti-cancer, microonde, cellules JF305, apoptose., Introduction Pancreatic cancer is one of the most lethal human malignancies, with a mortality rate of up to 96%. Pancreatic adenocarcinoma is locally invasive and is surrounded by a dense [...]

Induction of apoptosis in tumor cells has become the major focus of anti-tumor therapeutics development. Juglone, a major chemical constituent of Juglans mandshurica Maxim, possesses several bioactivities, including anti-tumor. In the present study, HeLa cells were incubated with juglone at various concentrations. The proliferation inhibition of juglone on HeLa cells was tested by the MTT assay. Occurrence of apoptosis was detected by Hoechst 33258 staining, flow cytometry, and transmission electron microscopy. The expression of apoptotic-related proteins was examined by Western blot. The results showed that juglone inhibits the growth of HeLa cells in dose--dependent manner. Topical morphological changes of apoptotic body formation after juglone treatment were observed. The percentages of early apoptosis of Annexin V-FITC were 5.23%, 7.95%, 10.69%, and 20.92% with the concentrations of juglone (12.5, 25, 50, and 100 (µmol/L), respectively. After cells were treated with juglone at the different dose for 24 h, the expression of Bcl-2 was significantly down-regulated and the expression of Bax was significantly up-regulated compared with the control. These events paralleled with activation of caspase-9, -8, -3, and PARP cleavage. The results suggest that juglone may be effective for the treatment of HeLa cells. Key words: anticancer, juglone, HeLa cells, apoptosis, cytotoxicity, caspases, early apoptosis. L'induction de l'apoptose des cellules tumorales est devenu un element central du developpement de therapies anti-tumorales. La juglone, la constituante chimique principale de Juglans mandshurica Maxim, possede plusieurs activites biologiques dont une activite anti-tumorale. Dans cette etude, des cellules HeLa ont ete incubees avec differentes concentrations de juglone. L'inhibition de la proliferation des cellules HeLa par la juglone a ete mesuree par le dosage de MTT. L'apoptose a ete detectee par une coloration au Hoechst 33258, par cytometrie de flux et par microscopie electronique a transmission. L'expression de proteines reliees a l'apoptose a ete examinee par buvardage Western. Les resultats ont montre que la juglone inhibe la croissance des cellules HeLa de facon dependante de la concentration. Des changements morphologiques locaux dans la formation de corps apoptotiques a la suite du traitement a la juglone ont ete observes. Les pourcentages d'apoptose precoce detectes par la coloration a l'annexine V-FITC etaient de 5,23 %, 7,95 %, 10,69 % et 20,92 % a des concentrations de 12,5 , 25 , 50 et 100 (µmol/L de juglone, respectivement. Apres que les cellules aient ete traitees aux differentes concentrations de juglone pendant 24 h, l'expression de Bcl-2 etait significativement diminuee et l'expression de Bax etait significativement regulee a la hausse comparativement aux controles. Ces evenements se deroulaient parallelement a l'activation des capsases 9, 8 et 3 ainsi qu'au clivage de la PARP. Ces resultats suggerent que la juglone peut etre efficace dans le traitement des cellules HeLa. Mots-cles : anti-cancer, juglone, cellules HeLa, apoptose, cytotoxicite, caspases, apoptose precoce. [Traduit par la Redaction], Introduction Human cervical cancer is a major mortality factor in the female population. HeLa cell (also Hela or hela cell) is a cell type in an immortal cell line used [...]

Ref.: Can. J. Physiol. Pharmacol. 92(4): 324-329 (2014). The statement informing that Wenhe Zhu and Wei Zhang contributed equally to this work was left out of the original published version. [...]

An artificial semisynthetic material can be derived from artemisinin (ART) called dihydroartemisinin (DHA). Although DHA has enhanced antigiardial potential, its clinical application is limited because of its poor selectivity and low solubility. The drug's absorption has a direct impact on the cell, and mechanism research is limited to its destruction of the cytoskeleton. In this study, we used the zeolitic imidazolate framework-8 and loaded it with DHA (DHA@Zif-8) to improve its antigiardial potential. DHA@Zif-8 can enhance cellular uptake, increase antigiardial proliferation and encystation, and expand the endoplasmic reticulum compared with the DHA-treated group. We used RNA sequencing (RNA-seq) to investigate the antigiardial mechanism. We found that 126 genes were downregulated and 123 genes were upregulated. According to the KEGG and GO pathway analysis, the metabolic functions in G. lamblia are affected by DHA@Zif-8 NPs. We used real-time quantitative reverse transcription polymerase chain reaction to verify our results using the RNA-seq data. DHA@Zif-8 NPs significantly enhanced the eradication of the parasite from the stool in vivo . In addition, the intestinal mucosal injury caused by G. lamblia trophozoites markedly improved in the intestine. This research provided the potential of utilizing DHA@Zif-8 to develop an antiprotozoan drug for clinical applications., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Jiang, Li, Liu, Sun, Zheng, Wan, Zhu and Feng.)

Objective: To investigate the cardiac injury effect of different intensities microwave radiation on rabbits and its possible mechanism., Methods: Rabbits were radiated by intensity of 50, 100, 150 and 200 mW/cm2 2450 MHz microwave for 20 min. 6 h after microwave radiation, the heart tissue was taken. ATP and mitochondria complex IV and V were measured in myocardial cells. The changes of myocardial tissue were observed by light microscopic. The expression of Caspase-3 and HSP 70 were detected by western blotting., Results: The activity of ATP and mitochondria complex IV and V decreased significantly compared with normal control in cardiac tissue. 100, 150 and 200 mW/cm2 microwave radiation group vs. control group (P <0. 05). The HE staining result showed that myocardial cell appears edema, muscle fiber malalignment, cells appeared obvious injury. Results of western blotting showed that the expression of Caspase-3 and HSP 70 protein increased significantly in different dosage radiation group (P <0. 05)., Conclusion: Microwave radiation has injury effect on rabbit heart. The possible mechanism may be related with inducing cell apoptosis by changing of stress level in myocardial cell.

Objective: To explore the effect of juglone on proliferation and apoptosis of human cervical squamous cancer SiHa cells., Methods: Cultured SiHa cells in the exponential growth phase were grouped into blank control group and 10, 20, 50, 80 and 100 μmol/L juglone treatment groups. Methyl thiazolyl tetrazolium (MTT) assay was adopted to observe the inhibitory effect of juglone on the proliferation of SiHa cells, and then 50% inhibitory concentration (IC50) was calculated through formula. Annexin V-FITC/PI double staining and flow cytometry were used to detect the effect of 20 μmol/L juglone on SiHa cell apoptosis. Western blot was applied to determine the expressions of Bcl-2 and Bax., Results: MTT assay showed that, compared with the control group, treatment groups all showed significant inhibitory effects on SiHa cell growth, and IC50 was 20.4 μmol/L. Flow cytometry demonstrated that early apoptosis rate of SiHa cells in the control group was (2.46 ± 0.37)%, and after treatment with 20 μmol/L Juglone for 12 hours, the apoptosis rate was raised to (18.47 ± 2.26)%; Western blot analysis showed that the expression of Bcl-2 decreased while the expression of Bax increased significantly in SiHa cells treated with 20 μmol/L juglone., Conclusion: Juglone could significantly inhibit the proliferation and induce the apoptosis of SiHa cells.

Objective: To explore the effects of Juglone on proliferation and apoptosis of human cervical cancer Caski cells, and to further study the related mechanism of cell apoptosis., Methods: Cultured Caski cells were incubated with 20, 40, 60, 80 and 100 μmol/L juglone for 24 h. The proliferation of Caski cells was detected by methyl thiazolyl tetrazolium (MTT) assay. The cell apoptosis were detected by transmission electron microscope. The expression of Bcl-2 and Bax were detected by Western blot., Results: MTT results showed that in different doses of juglone groups, the Caski cell growth was greatly inhibited (P < 0.05, P < 0.01) and showed dose dependent when compared with control group except 20 μmol/L. The IC50 of juglone was 42.4 μmol/L. After treatment on Caski cells with 40 μmol/L juglone, typical apoptosis characteristics was observed by transmission electronmicro scope. The expression of Bcl-2 was decreased while the expression of Bax was increased significantly when compared with control group (P < 0.05)., Conclusion: Juglone significantly inhibits the proliferation and induces the apoptosis of Caski cells in vitro.

Objective: To investigate on the proliferation effect of different intensities 2450 MHz microwave radiation on human pancreatic cancer JF305 cells and its possible mechanism., Methods: JF305 cells were radiated by intensity of 2.5, 5.0, 10.0, 15.0 and 20.0 mW/cm2 microwave for 20 min. The proliferation capacity of JF305 was measured by MTT assays, Annexin V-FITC and PI staining was used for detecting cell apoptosis. The activity of Caspase-3 was examined. The expressions of Caspase-3 and HSP 70 protein after the cell treatment with microwave were detected by Western blotting., Results: After microwave radiation, the proliferation inhibition rates of JF305 cells were significantly higher compared with control group. Annexin V-FITC and PI staining result showed that microwave radiation could induce cell apoptosis. Caspase-3 increased after radiated by microwave, compared with control group (P < 0.05). Results of Western blotting showed that the expression of Caspase-3 and HSP 70 protein increased significantly in different dosage radiation group., Conclusion: Microwave radiation can inhibit the proliferation of JF305 cells, the possible mechanism may be related with inducing cell apoptosis by changing of stress level.