scholarly journals Effects of sodium alendronate on osteoporosis and apoptosis-related factors Cyt C, Apaf-1 and caspase-9

2018 ◽  
Vol 29 (3) ◽  
Author(s):  
Hong Li ◽  
Chunde Li ◽  
Xiaodong Yi ◽  
Hong Liu ◽  
Yu Wang
Keyword(s):  
Caspase 9 ◽  
Related Factors ◽  
Cyt C

Real-Time In Situ Sequential Fluorescence Activation Imaging of Cyt c and Caspase-9 with a Gold–Selenium-Bonded Nanoprobe

2021 ◽  
Author(s):  
Bo Liu ◽  
Jingjing Li ◽  
Ping Zhou ◽  
Wei Pan ◽  
Na Li ◽  
...  
Keyword(s):  
Real Time ◽  
Caspase 9 ◽  
Cyt C

TRIAP1 Inhibition Activates the Cytochrome c/Apaf-1/Caspase-9 Signaling Pathway to Enhance Human Ovarian Cancer Sensitivity to Cisplatin

Chemotherapy ◽  
2019 ◽  
Vol 64 (3) ◽  
pp. 119-128 ◽  
Author(s):  
Tian-Mei Zhang
Keyword(s):  
Ovarian Cancer ◽  
Nude Mice ◽  
Cell Apoptosis ◽  
Caspase 9 ◽  
Ovarian Carcinoma Cell Line ◽  
Skov3 Cells ◽  
Cyt C ◽  
Sirna Group

Objective: To investigate whether TRIAP1inhibition affects the ovarian cancer cell resistance to cisplatin (DDP) via the Cyt c/Apaf-1/caspase-9 pathway by in vitro and in vivo experiments. Methods: CCK8 assay was performed to find out how treatment with both TRIAP1 siRNA and DDP affects the cell viability of SKOV3 cells and DDP-resistant human ovarian carcinoma cell line SKOV3/DDP. SKOV3/DDP cells were transfected with control siRNA or TRIAP1 siRNA before 24 h of treatment with DDP (5 μg/mL). Flow cytometry was employed to detect cell apoptosis and Western blot to examine the expressions of Cyt c/Apaf-1/caspase-9 pathway-related proteins. SKOV3/DDP cells transfected with control siRNA or TRIAP1 siRNA were subcutaneously injected into BALB/c-nu/nu nude mice followed by the intraperitoneal injection of DDP (4 mg/kg). Cyt c/Apaf-1/caspase-9 pathway in transplanted tumors was detected by immunohistochemistry. Results: TRIAP1 expression declined in SKOV3 cells when compared with SKOV3/DDP cells. The proliferation rate was lower in SKOV3/DDP cells transfected with TRIAP1 siRNA combined with treatment of DDP (1, 2, 4, 6, 8, 16, 32 μg/mL) than in those transfected with control siRNA. Moreover, the TRIAP1 siRNA group had an increased SKOV3/DDP cell apoptosis rate with the activation of the Cyt c/Apaf-1/caspase-9 pathway. During DDP treatment, nude mice in TRIAP1 siRNA group had slower growth and smaller size of transplanted tumor than those in control siRNA group, with increased expression of Cyt c, Apaf-1, and caspase-9. Conclusion: TRIAP1 inhibition may enhance the sensitivity of SKOV3/DDP cells to cisplatin via activation of the Cyt c/Apaf-1/caspase-9 pathway.

scholarly journals Mechanism of Heshouwuyin inhibiting the Cyt c/Apaf-1/Caspase-9/Caspase-3 pathway in spermatogenic cell apoptosis

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Hongjie Wang ◽  
Juan Zhu ◽  
Liping Jiang ◽  
Boying Shan ◽  
Peihan Xiao ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Caspase 3 ◽  
Spermatogenic Cell ◽  
Caspase 9 ◽  
Cyt C

scholarly journals Ameliorative Effects of Nano-Selenium Against Fluoride Stress Induced Hepatocytes Autophagy and Apoptosis in Mice

2020 ◽  
Author(s):  
Yajing Wang ◽  
Bingxian Liu ◽  
Qingyue Han ◽  
Khalid Mehmood ◽  
Fazul Nabi ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Beclin 1 ◽  
Protective Effects ◽  
Human Beings ◽  
Caspase 9 ◽  
Nano Material ◽  
Cyt C ◽  
Hepatocyte Damage

Abstract Background: Fluorine is widespread in the environment, and the injurious impacts of fluoride underscore its significance for public health. The long-term presence of fluorine in environment could be a risk in hepatotoxicity for both human beings and animals. Important role of selenium in mitigation of heavy metal toxicity via regulating autophagy and apoptosis is well-known. Further, nano-Se is a common artificial nano material, with higher biological activity and lower toxicity. The aim of the current study was to examine whether nano-Se supplementation can reduce the effects of fluoride-induced hepatocytes autophagy and apoptosis. Results: Here, we report that fluoride exposure induces apoptosis and autophagy with nucleus broken, dissolved and disappeared of hepatocyte, contributing to its hepatotoxicity. More importantly, Cyt-C and Beclin-1/Bcl-2 pathways are involved in the regulation of autophagy and apoptosis via targeting Caspase-9, Caspase-3, P53, Bax, LC3, ATG-5, P62 and mTOR expressions. Conclusion: Nano-Se is capable to alleviate fluoride-induced hepatocyte damage, that selenium can be prefer to prevent chronic fluorosis-induced autophagy and apoptosis by regulating Cyt-C and Beclin-1/Bcl-2 signaling pathway. In precisely, NaF-induced the liver injury by activating autophagy and apoptosis, which indicate that fluorine exposure, pose an ecological risk to human beings and animals. Nano-Se has protective effects against fluoride-induced hepatocytes.

scholarly journals Molecular mechanism of mice gastric oxidative damage induced by nanoparticulate titanium dioxide

2021 ◽  
Author(s):  
Jianhui Ji ◽  
Yingjun Zhou ◽  
Fashui Hong ◽  
Yuguan Ze ◽  
Dongxue Fan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Titanium Dioxide ◽  
Antioxidant Enzymes ◽  
Molecular Mechanisms ◽  
Intragastric Administration ◽  
Nano Tio2 ◽  
Related Factors ◽  
Atp Production ◽  
Cyt C

Abstract Background Nanoparticulate titanium dioxide (Nano-TiO2) has been widely used in food industry, and it has been demonstrated to have adverse effects on mice and human stomach, but its mechanism is rarely concerned. The aim of this study is to determine the effects of nano-TiO2 on the stomach and confirm the role of oxidative stress and apoptosis in the mice gastric damage caused by nano-TiO2, as well as its molecular mechanisms. Methods Mice were continuously exposed to nano-TiO2 with 1.25, 2.5 and 5 mg/kg bw by intragastric administration for 9 months in the present study. The ultrastructure, levels of reactive oxygen species (ROS) and peroxides, activities of antioxidant enzymes and mitochondria-related enzymes, ATP contents as well as apoptosis-related factors expression in mice stomach were examined. Results Oxidative stress, apoptosis and nano-TiO2 aggregation were found in gastric mucosal smooth muscle cells after nano-TiO2 exposure. Nano-TiO2 exposure also resulted in the over-production of ROS and peroxides, decrease of ATP production and activities of antioxidant enzymes and mitochondria-related ATPases, upregulation of apoptosis-related factors including γH2AX, Cyt c, caspase 3, and p-JNK expression, and down-regulation of Bcl-2 expression in mice stomach. Conclusions The gastric toxicity of mice induced by chronic exposure to low dose nano-TiO2 may be associated with oxidative stress and mitochondria-mediated apoptosis in mice.

scholarly journals Effect of Andrographis paniculata polysaccharide on human retinoblastoma Y79 cell proliferation and apoptosis

2021 ◽  
Vol 14 (4) ◽  
pp. 497-503
Author(s):  
Bing Xu ◽  
◽  
Wei Zhang ◽  
Yue Li ◽  
Mao-Ren Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Signal Pathway ◽  
Caspase 8 ◽  
Caspase 9 ◽  
Related Factors ◽  
Proliferation And Apoptosis ◽  
Human Retinoblastoma ◽  
Y79 Cells

AIM: To explore the effect of the Andrographis paniculata (A. paniculata) polysaccharide on the proliferation and apoptosis of human retinoblastoma (RB) Y79 cells and its mechanism. METHODS: The refined A. paniculata polysaccharide was obtained using techniques such as water extraction, ethanol precipitation, and decompression concentration. The inhibition effect of the A. paniculata polysaccharide on the proliferation of Y79 cells was detected by cell proliferation assay. Flow cytometry was used for the detection of cell apoptosis rate and cycle change. Real-time qunatitative polymerase chain reaction (RT qPCR)and Western blotting were used to detect the expression of cell apoptosis signal pathway-related factors (caspase-3, caspase-8, and caspase-9) and cell cycle signal pathway-related factors (CDK1 and cyclinB1) at the transcriptional and translational levels. RESULTS: Infrared and ultraviolet spectrum scanning showed that the extracted drug was a polysaccharide with high purity. After being treated with different concentrations of A. paniculata polysaccharide for different periods of time, the Y79 cells showed different degrees of proliferation inhibition. Flow cytometric observations showed that the cell apoptosis rate and the proportion of cells blocked in the G2/M phase were significantly increased after A. paniculata polysaccharide treatment. Further analysis revealed that the mRNA and protein expression of caspase-3, caspase-8, and caspase-9 in the A. paniculata polysaccharide treatment groups increased significantly compared with that in the control groups, while the expression of CDK1 and cyclinB1 decreased significantly. CONCLUSION: The A. paniculata polysaccharide could inhibit the proliferation and induce apoptosis of Y79 cells. Its possible mechanism is via the upregulation of caspase-3, caspase-8, and caspase-9 expression in the cell apoptotic signaling pathway and the downregulation of CDK1 and cyclinB1 expression in the cell cycle signaling pathway.

scholarly journals Electroacupuncture Pre-treatment Exerts an Anti-apoptotic Effect in Cerebral Ischaemia and Reperfusion Injury in Rats

2021 ◽  
Author(s):  
Zhu Luwen ◽  
Ye Tao ◽  
Tang Qiang, ◽  
Yan Wang ◽  
Li Hongyu ◽  
...  
Keyword(s):  
Cerebral Ischaemia ◽  
Neurological Deficits ◽  
Tunel Staining ◽  
Caspase 9 ◽  
Brain Infarct ◽  
Severity Scores ◽  
Ischaemia And Reperfusion ◽  
Apoptotic Effect ◽  
Cyt C ◽  
Pre Treatment

Background: Electroacupuncture (EA) pre-treatment can play a significant neuroprotective role in rats with cerebral ischaemia and reperfusion (CIR) injury, but the specific mechanism needs to be further elucidated. <br><br>Objective: To investigate the effects of EA pre-treatment on apoptosis-related proteins Bax, Bcl-2, Cytochrome c (cyt c), cleaved caspase-9 and -3 in rats with CIR injury. Methods: CIR injury was induced using middle cerebral artery occlusion (MCAO) ischaemia-reperfusion. Thirty-six male Specific Pathogen Free (SPF) Sprague-Dawley rats were randomly divided into three groups: Sham (n=12), MCAO (n=12), and the EA+MCAO group (n=12). EA+MCAO group rats received electroacupuncture at DU20 for 2 consecutive weeks before MCAO model preparation. After 24 h of reperfusion, neurological deficits were evaluated by modified neurological severity scores. Brain infarct volumes were examined by 2,3,5-triphenyltetrazolium chloride staining. Expression of Bax, Bcl-2, cyt c, cleaved caspase-9 and -3 in the ischaemic penumbra were detected by Western blotting, and apoptosis evaluated by TUNEL staining. <br><br>Results: After perfusion for 24 h, compared with the MCAO group, the neurological deficit scores and brain infarct volumes in the EA+MCAO group were significantly decreased (P<0.05), as was the level of Bax (P<0.05) or the Bax/Bcl-2 ratio (P<0.05), levels of cyt c, cleaved caspase-9 and -3 also decreased (P<0.05), like the number of TUNEL-positive cells (P<0.05), in contrast, the level of Bcl-2 increased (P<0.05). <br><br>Conclusion: EA pre-treatment exerts an anti-apoptotic effect through Bax-to-Bcl-2 ratio downregulation, blockage of mitochondrial cyt c release to the cytosol, and reduction of caspase-9 and -3 expression in rats with CIR injury.

scholarly journals Effects and Mechanism of Berberine on the Dexamethasone-Induced Injury of Human Tendon Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Shangjun Fu ◽  
Zongyun He ◽  
Yongfeng Tang ◽  
Bo Lan
Keyword(s):  
Oxidative Stress ◽  
Flow Cytometry ◽  
Cell Migration ◽  
Caspase 3 ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Caspase 9 ◽  
Related Factors ◽  
Tendon Cells ◽  
Human Tendon

Objective. To investigate the effects of berberine (Berb) on dexamethasone- (Dex-) induced injury of human tendon cells and its potential mechanism. Methods. CCK-8 assay was used to explore the appropriate concentration of Dex-induced injury of tendon cells and the doses of Berb attenuates Dex cytotoxicity; cell wound healing assay was used to detect the effects P < 0.05 of Berb and Dex on the migration ability of tendon cells; flow cytometry was used to measure cell apoptosis; DCF DA fluorescent probe was used to measure the ROS activity of cells. Western blotting was used to detect the expression of phenotype related factors including smooth muscle actin α (SMA-α), type I collagen (Col I), col III, apoptosis-related factors, caspase-3, cleaved caspase-3, caspase-9, cleaved caspase-9, and PI3K/AKT. Results. CCK-8 assay showed that 1–100 μM Dex significantly inhibited the proliferation of tendon cells in a concentration-dependent manner P < 0.05 , where the inhibitory effect of 100 μM Dex was most significant P < 0.005 , and the pretreatment of 150, 200 μM Berb could reverse those inhibitions (all P < 0.05 ). Compared with the control group, Dex significantly inhibited cell migration P < 0.05 , while Berb pretreatment could enhance cell migration P < 0.05 . Flow cytometry and ROS assay showed that Dex could induce apoptosis and oxidative stress response of tendon cells (all P < 0.05 ), while Berb could reverse those responses P < 0.05 . Western blot showed that Dex could inhibit the expression of the col I and III as well as α-SMA (all P < 0.05 ) and enhance the expression of apoptosis-related factors including cleaved caspase-3 and cleaved caspase-9 (all P < 0.05 ). Besides, Dex could also inhibit the activation of the PI3K/AKT signaling pathway (all P < 0.05 ), thus affecting cell function, while Berb treatment significantly reversed the expression of those above proteins (all P < 0.05 ). Conclusion. Berb attenuated DEX induced reduction of proliferation and migration, oxidative stress, and apoptosis of tendon cells by activating the PI3K/AKT signaling pathway and regulated the expression of phenotype related biomarkers in tendon cells. However, further studies are still needed to clarify the protective effects of Berb in vivo.

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