scholarly journals Emodin induces Panc-1 cell apoptosis via declining the mitochondrial membrane potential

2012 ◽  
Vol 28 (6) ◽  
pp. 1991-1996 ◽  
Author(s):  
JIN-XIANG LIU ◽  
JIAN-HONG ZHANG ◽  
HONG-HAI LI ◽  
FU-JI LAI ◽  
KANG-JIE CHEN ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Cell Apoptosis ◽  
Mitochondrial Membrane

scholarly journals Artemisinin attenuated oxidative stress and apoptosis by inhibiting autophagy in MPP+-treated SH-SY5Y cells

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Junqiang Yan ◽  
Hongxia Ma ◽  
Xiaoyi Lai ◽  
Jiannan Wu ◽  
Anran Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Protein Expression ◽  
Mitochondrial Membrane Potential ◽  
Western Blotting ◽  
Cell Apoptosis ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Neuroprotective Effects

Abstract Background Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease. The oxidative stress is an important component of the pathogenesis of PD. Artemisinin (ART) has antioxidant and neuroprotective effects. The purpose of this study is to explore the neuroprotective effect of ART on 1-methyl-4-phenyliodine iodide (MPP +)-treated SH-SY5Y cells and underlying mechanism. Methods We used MPP+-treated SH-SY5Y cells to study the neuroprotective effect of ART. Cell viability was measured by MTT assay after incubating the cells with MPP+ and/or ART for 24 h. DCFH-DA was used to detect the level of intracellular reactive oxygen species (ROS), and WST-8 was used to detect the level of superoxide dismutase (SOD). The level of intracellular reduced glutathione (GSH) was detected with 5,5΄-dithiobis-(2-nitrobenzoic acid), and the level of malondialdehyde (MDA) was assessed based on the reaction of MDA and thiobarbituric acid. A mitochondrial membrane potential detection kit (JC-1) was used to detect changes in the mitochondrial membrane potential (MMP), and an Annexin V-FITC cell apoptosis kit was used to detect cell apoptosis. The expression levels of caspase-3, cleaved caspase-3 and the autophagy-related proteins LC3, beclin-1, and p62 were detected by Western blotting. In addition, to verify the change in autophagy, we used immunofluorescence to detect the expression of LC3 and p62. Results No significant cytotoxicity was observed at ART concentrations up to 40 μM. ART could significantly increase the viability of SH-SY5Y cells treated with MPP+ and reduce oxidative stress damage and apoptosis. In addition, the Western blotting and immunofluorescence results showed that MPP+ treatment could increase the protein expression of beclin1 and LC3II/LC3I and decrease the protein expression of p62, indicating that MPP+ treatment could induce autophagy. Simultaneous treatment with ART and MPP+ could decrease the protein expression of beclin1 and LC3II/LC3I and increase the protein expression of p62, indicating that ART could decrease the level of autophagy induced by MPP+. Conclusion Our results indicate that ART has a protective effect on MPP+-treated SH-SY5Y cells by the antioxidant, antiapoptotic activities and inhibition of autophagy. Our findings may provide new hope for the prevention and treatment of PD.

scholarly journals Effects of Berberine on Cell Cycle, DNA, Reactive Oxygen Species, and Apoptosis in L929 Murine Fibroblast Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Manman Gu ◽  
Jing Xu ◽  
Chunyang Han ◽  
Youxi Kang ◽  
Tengfei Liu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Dna Damage ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Cell Apoptosis ◽  
Mitochondrial Membrane ◽  
Oxygen Species ◽  
Cycle Arrest ◽  
Murine Fibroblast

Berberine, an isoquinoline alkaloid isolated from several traditional Chinese herbal medicines (TCM), exhibits a strong antimicrobial activity in the treatment of diarrhea. However, it causes human as well as animal toxicity from heavy dosage. The present study was conducted to investigate the cytotoxicity of berberine and its possible trigger mechanisms resulting in cell cycle arrest, DNA damage, ROS (reactive oxygen species) level, mitochondrial membrane potential change, and cell apoptosis in L929 murine fibroblast (L929) cells. The cells were culturedin vitroand treated with different concentrations of berberine for 24 h. The results showed that cell viability was significantly decreased in a subjected dose-dependent state; berberine concentrations were higher than 0.05 mg/mL. Berberine at a concentration above 0.1 mg/mL altered the morphology of L929 cells. Cells at G2/M phase were clear that the level of ROS and cell apoptosis rates increased in 0.1 mg/mL group. Each DNA damage indicator score (DIS) increased in groups where concentration of berberine was above 0.025 mg/mL. The mitochondrial membrane potential counteractive balance mechanics were significantly altered when concentrations of berberine were above 0.005 mg/mL. In all, the present study suggested that berberine at high dosage exhibited cytotoxicity on L929 which was related to resultant: cell cycle arrest; DNA damage; accumulation of intracellular ROS; reduction of mitochondrial membrane potential; and cell apoptosis.

Potential Crosstalk Of Ca2+-ROS Dependent Mechanism Involved In Kasumi cells’ Apoptosis Induced By Lentivirus-Mediated HO-1 siRNA

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 5558-5558
Author(s):  
Jishi Wang ◽  
Wei Sixi ◽  
Wang Yating ◽  
Chai Qixiang
Keyword(s):  
Membrane Potential ◽  
Cell Viability ◽  
Mitochondrial Membrane Potential ◽  
Cell Apoptosis ◽  
Mitochondrial Membrane ◽  
The Other ◽  
Ros Generation ◽  
Dependent Manner ◽  
Realtime Pcr ◽  
Protein Expressions

Abstract Aim Using lentivirus-mediated HO-1 siRNA (lenti-siHO-1-GFP) to silence the HO-1 gene in Kasumi cells so as to explore the role and mechanism of HO-1 on cell apoptosis. Methods To infect Kasumi cells with lenti-siHO-1-GFP and check the infection efficiency by using fluorescence microscopy and flow cytometry (FCM). Experimental group was divided into three groups: untreated Kasumi (K), infected Kasumi by empty vector (lenti-GFP-K) and infected Kasumi by lentivirus-mediated HO-1 siRNA (lenti-siHO-1-K). The HO-1 expression of each group was detected by realtime PCR. Fluo3-AM method was used to detect the intracellular Ca2+ accumulation. DCFH-DA was used for the measurement of intracellular ROS. The change of mitochondrial membrane potential was evaluated by JC-1 stainning by using FCM. After being treated with various concentrations of daunorubicin for 24, 48, and 72 h respectively, cell viability was determined by MTT assay. Cell apoptosis was determined by FCM following with cells dual-stained with Annexin-V-FITC and propidium iodide (PI). The mRNA of HO-1 and apoptosis-related genes were analyzed by realtime PCR and, the expressions of their corresponding protein were determined by western blot. Additionally, After treating with 10mM Ca2+chelator BAPTA-AM and 0.5mM NAC for 12h, Ca2+ accumulation, ROS generation, the expression of HO-1 and apoptosis-related genes were detected respectively. Result presented in mean±sd manner. Results After lenti-siHO-1-GFP infection for 48h, we could observe the fluorescence clear, the fluorescent intensity was 95.87% after 72 hours. The HO-1 silencing efficiency of lenti-siHO-1-K was 77.00%. MTT result showed that daunorubicin exerted moderate inhibitory effects on cell proliferation in a dose and time dependent manner. With the same treating conditions, the cell viability of lenti-siHO-1-K group was significantly lower than the other two groups(e.g 49.20±1.30% survival in lenti-siHO-1-K group, 72.40±1.90% in K group and 74.10±2.10% in lenti-GFP-K group after being treated by 5ug/ml DNR,respectively, p=0.014), while the apoptosis rate was higher than the other two groups(e.g 75.77±3.41% in lenti-siHO-1-K group, 23.72±2.03% in K group and 26.10±1.95% in lenti-GFP-K group after being treated by 5ug/ml DNR,respectively, p=0.011). Compared with other two groups, the lenti-siHO-1-K group showed a downregulation in the mRNA and protein expression of HO-1. The mRNA and protein expressions of cyto-C, caspase3, caspase8, caspase9 and caspase12 in lenti-siHO-1-K group were upregulated after exposure to 5ug/ml daunorubicin for 24 hours. Compared with K and lenti-GFP-K groups, Ca2+ accumulation in lenti-siHO-1-K group was increased significantly(e.g 40.35±2.10% in lenti-siHO-1-K group, 17.30±1.81% in K group and 14.15±1.75% in lenti-GFP-K group,respectively, p=0.041). The ROS generation was higher than the other two groups(e.g 47.65±2.05% in lenti-siHO-1-K group, 21.30±1.94% in K group and19.90±2.01% in lenti-GFP-K group,respectively, p=0.037). The ratio of Green/Red fluorescence intensity increased significantly in lenti-siHO-1-K group(e.g 0.704±0.06 in lenti-siHO-1-K group, 0.57±0.09 in K group and 0.527±0.05 in lenti-GFP-K group, respectively, p=0.042). After exposure to 10mM BAPTA-AM and 0.1mM NAC alone or combined with, both the intracellular Ca2+accumulation and the ROS level in lenti-siHO-1-K group reduced(17.59±1.01% of Ca2+acumulation and 19.78±1.3% of ROS production after BAPTA-AM treatment alone, 23.42±1.97% of Ca2+and 15.47±1.14% of ROS after being treated by NAC alone, 16.52±1.23% of Ca2+and 14.37±1.21% of ROS after treatment by both agent) , while the mRNA and protein expressions of cyto-C, caspase3, caspase8, caspase9 and caspase12, decreased significantly. Conclusion HO-1 gene silencing played a role in pro-apoptosis in Kasumi cells. The mechanism may be related to the endoplasmic reticulum stress and abnormal accumulation of intracellular Ca2+, ROS generation, descending of the mitochondrial membrane potential and release cyto-C, then further activated the caspases cascade and promoted apoptosis. However, it tended to be initiated by crosstalk in Ca2+-ROS pathway. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Germinated Brown Rice Protects H9c2 Cardiomyocyte against Simulated Ischemic/Reperfusion Injury via Mediated Mitochondria Function

2020 ◽  
Author(s):  
Kanokwan Demeekul ◽  
Wichit Suthammarak ◽  
Soontaree Petchdee
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Cell Apoptosis ◽  
Mitochondrial Membrane ◽  
Brown Rice ◽  
Germinated Brown Rice ◽  
H9c2 Cardiomyocytes ◽  
Cardioprotective Effects

Abstract Background Ischemia/reperfusion (I/R) injury is the major mechanism during Ischemic Heart Disease (IHD). The key modulator of I/R injury is dysregulation of mitochondria function. Germinated Brown Rice (GBR) has recommended as a bio-functional food and has clarified the potential properties in several effects. However, the effect of GBR mediated cardioprotective properties, focusing on the role of mitochondrial function, remains unexplored. Thus, this study aims to investigate the cardioprotective effects of GBR pretreatment against simulated I/R injury. Results H9c2 cardiomyocytes were incubated with GBR at a concentration of 5 ƞg/ml for 24 hours and/or simulated I/R (sI/R) for 40 minutes. Cell viability and cell apoptosis were assessed by 7-AAD staining and AnnexinV/PI staining, respectively. For evaluation of mitochondrial functions, not only mitochondrial membrane potential was determined by JC-1 staining but also mitochondrial respiration was represented by oxygen consumption rate (OCR) using Seahorse Flux analyzer. The results revealed that administration of GBR prior to sI/R significantly decreased the percentage of cell death and total cell apoptosis in H9c2 during stimulation of ischemic/reperfusion. In addition, pretreatment of cardiomyocytes with GBR remarkably stabilized mitochondrial membrane potential and improved impaired mitochondrial respiration in simulated-H9c2 injury. Conclusion the present research is the first study to report the effective cardioprotection of GBR. Pretreatment of GBR potentially protects H9c2 cardiomyocytes against sI/R injury through mitochondrial function. The underlying therapeutic activities are possibly associated with its bio-functional compounds. However, the underlying mechanism on cardioprotective effects of GBR needs further studies.

scholarly journals Caenorhabditis elegans ATPase inhibitor factor 1 (IF1) MAI-2 preserves the mitochondrial membrane potential (Δψm) and is important to induce germ cell apoptosis

PLoS ONE ◽  
2017 ◽  
Vol 12 (8) ◽  
pp. e0181984 ◽  
Author(s):  
L. P. Fernández-Cárdenas ◽  
E. Villanueva-Chimal ◽  
L. S. Salinas ◽  
C. José-Nuñez ◽  
M. Tuena de Gómez Puyou ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Caenorhabditis Elegans ◽  
Germ Cell ◽  
Mitochondrial Membrane Potential ◽  
Cell Apoptosis ◽  
Mitochondrial Membrane ◽  
Atpase Inhibitor ◽  
Germ Cell Apoptosis
Sign in / Sign up

Export Citation Format

Share Document