Showing 6 results for Apoptosis
Seyedeh Tahereh Haeri, Mohammad Ali Azarbayjani, Maghsoud Peeri,
Volume 13, Issue 4 (7-2019)
Abstract
Background and Objectives: Apoptosis is essential for the survival and normal functioning of multicellular organisms, yet any interruption in this process could be detrimental. Increased production of reactive oxygen species and oxidative stress are key factors affecting apoptosis. Our objective was to determine the impact of exercise with and without vitamin D supplementation on expression of FLIP, Fas, and caspase 8 in lung of rats poisoned with H2O2.
Methods: Forty-eight adult male rats were randomly divided into six groups: (C), (H), (HD), (HE), (HDE) and dimethyl sulfoxide. Groups H, HE, HD and HDE received 1 mmol/Kg intraperitoneal injection of H2O2. HE and HDE groups ran on treadmill for eight weeks. Expression of FLIP, Fas and caspase 8 was measured in lung tissues using RT-qPCR. Statistical analysis of data was carried out using SPSS 22 at significance level of 0.05.
Results: Vitamin D supplementation caused a significant decrease in expression of Fas (P=0.014) and caspase 8 (P=0.016) compared to the control group. However, it significantly overexpressed FLIP in the lung tissues compared to the control group (P=0.005). Exercise with and without vitamin D supplementation had no significant effect on the expression of the apoptosis regulatory genes.
Conclusion: Our results show that VD exerts protective effects on lung tissue by regulating apoptotic factors. Aerobic exercise alone and combined with VD has no significant effect on the apoptotic factors. These results indicate that VD supplementation can reduce lung injury under oxidative stress conditions.
Somayeh Ramezani, Maghsoud Peeri, Mohammad Ali Azarbaijani, Firoozeh Dehghan,
Volume 13, Issue 5 (9-2019)
Abstract
ABSTRACT
Background and Objectives: Exercise is a strong physiological stimulus that can affect apoptosis in the lungs by altering a number of extracellular and intracellular signaling pathways. The present study examined effects of regular aerobic exercise and vitamin D on expression of Bcl-2, Bax and caspase-3 in lung tissues of male rats exposed to hydrogen peroxide.
Methods: Forty-eight adult male Wistar rats were randomly assigned into six groups of eight, including 2 x H 2 O 2, 2H 2 O 2, Vit D (2HD), 2H2O2 + Regular Exercise Training (2HE), 2H2O2 + D3 + E (2HDE) ; Dimethyl sulfoxide (DMSO) and control (C). Subjects in the training groups performed aerobic exercise for eight weeks. Bax, Bcl-2, caspase-3 expression in the lung tissues was measured using RT-PCR.
Results: Bcl-2 expression in the exercise (P = 0.004) and vitamin D (P = 0.006) groups increased significantly compared to the control groups. Bax, Bcl-2 and caspase-3 expression was significantly lower in the exercise group and vitamin D supplementation group compared to the control group. On the other hand, concurrent exercise and vitamin D significantly reduce Bax expression but had no significant effect on Bcl-2 and caspase-3 expression.
Conclusion: Our results demonstrate that regular aerobic exercise along with vitamin D supplementation may play a role in reducing apoptosis in lungs following severe oxidative stress.
Keywords: Apoptosis, Bcl-2, Bax, Caspase3, Aerobic Exercise, Vitamin D
Esmaeil Khorshid Sofyani, Rasoul Sharifi,
Volume 14, Issue 4 (7-2020)
Abstract
Background and objectives: Combination chemotherapy with new adjuvants has been introduced as an innovative method of treating various types of cancer. The aim of this study was to investigate potential synergistic effect of quinacrine on the anti-proliferative and anti-apoptotic activity of docetaxel in
A549 lung cancer cells.
Methods: Cell viability and apoptosis percentage were evaluated with MTT assay and annexin V staining. To understand the mechanisms through which quinacrine modulates expression of pro-apoptotic and anti-apoptotic genes, expression of Bcl-2, Bcl-xl and Bax genes were investigated using
real-time RT-PCR.
Results: The half maximal inhibitory concentration values for docetaxel and quinacrine was 3.16±1.5 nM and 4.4±0.58 μM, respectively. The combination index value of docetaxel and quinacrine was 0.66 against A549 cells, indicating strong synergism. The expression of anti-apoptotic genes Bcl-2 and Bcl-xl reduced significantly, while the expression of the pro-apoptotic gene Bax increased significantly after co-treatment with docetaxel and quinacrine (P<0.05). Treatment of cells with a combination of quinacrine and docetaxel significantly increased the inhibitory effect of docetaxel (reduced proliferation by 50%) and the percentage of apoptotic cells.
Conclusion: Our findings suggest that the combination of quinacrine and docetaxel can be considered as a promising strategy for the treatment of patients with lung cancer.
Aghil Sadighi, Ahmad Abdi, Mohammad Ali Azarbayjani, Alireza Barari,
Volume 15, Issue 1 (1-2021)
Abstract
Background and objectives: Cardiac apoptosis is one of the most important cardiovascular complications of diabetes. We aimed to investigate the changes of Bax, Bcl2 and caspase 3 in cardiac tissue of diabetic rats after six weeks aerobic exercise.
Methods: Thirty two male Wistar rats were randomly divided into healthy control, diabetes control and diabetes + exercise groups. Diabetes was induced by intraperitoneal injection of streptozotocin solution (55 mg/kg). Two weeks after the injection, fasting blood glucose levels were measured to confirm induction of diabetes. The exercise program was performed five days a week for six weeks. Variables were evaluated by ELISA and western blot analysis. All statistical analyses were performed in SPSS (version 22) using ANOVA and at significance of 0.05.
Results: The induction of diabetes in the control groups resulted in a significant increase in Bax, Bax/Bcl2 ratio and a significant decrease in Bcl2 levels (P=0.024). The six-week training exercise in diabetic groups significantly decreased Bax and Bax/Bcl2 ratio and significantly increased Bcl2 (P=0.018).
Conclusion: Our finding showed that diabetes could increase apoptosis in cardiac tissue. In addition, the six-week aerobic exercise can be used as a non-pharmacological strategy to reduce diabetes-related apoptosis in cardiomyocytes.
Ali Nouri, Parvin Farzanegi, Mohammad Ali Azarbayjani,
Volume 16, Issue 4 (7-2022)
Abstract
Background and objectives: Diabetes mellitus is the most common metabolic disorder in the world. Here, we evaluated effects of resveratrol supplementation alone and combined with exercise on blood glucose, insulin, lipid profile, apoptosis biomarkers, and expression of farnesoid X receptor (Fxr), liver X receptor (Lxr), and sirtuin 1 (Sirt 1) genes in the liver of type 1 diabetic rats.
Methods: Streptozotocin was used to induce type 1 diabetes in Wistar rats. The rats were randomly assigned into seven groups. After treatment with resveratrol alone or combined with exercise training, the animals were sacrificed and lipid profile and levels of blood glucose and insulin were measured. Hepatocyte apoptosis was assessed by measuring the level of Bax and Bcl2 proteins using enzyme-linked immunosorbent assay kits. Expression of Fxr, Lxr, and Sirt1 was evaluated using real-time polymerase chain reaction. Comparison of the mean levels of all variables between different groups was performed using one-way analysis of variance, at statistical significance level of 0.05.
Results: Resveratrol significantly reduced the level of blood glucose and insulin compared with the control groups (p<0.001). It also significantly affected the lipid profile (p<0.001). Diabetes was significantly associated with decreased expression of Sirt1, Lxr, and Fxr and increased hepatocyte apoptosis. Resveratrol significantly improved the expression of all three genes (p<0.01). Overall, resveratrol supplementation combined with exercise was more effective than other methods.
Conclusion: The results indicate that that combination of resveratrol therapy with exercise could be beneficial for diabetic patients. However, more studies are needed to confirm this finding.
Mohadese Namjoo, Hossein Ghafoori, S. Mohsen Asghari,
Volume 17, Issue 1 (1-2023)
Abstract
Background and objectives: Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) inhibition results in an increase in apoptosis. It has been demonstrated that NF-κB subunit p65 phosphorylation at the IκB kinase phosphorylation site serine 536 (Ser536) is essential for the NF-κB nuclear translocation and activation. Therefore, NF-κB can be downregulated by suppressing its phosphorylation. The vascular endothelial growth factor receptor-2 (VEGFR-2) suppression could result in apoptosis induction. Therefore, targeting these pathways via VEGFR-2 inhibitors might have therapeutic potential for cancer treatment. It has been indicated that an antagonist peptide of VEGF, referred to as VGB3, could neutralize and recognize VEGFR2 in the tumoral and endothelial cells. This study aimed to induce apoptosis in human umbilical vein endothelial cells (HUVEC) cells through the inhibition of these signaling pathways.
Methods: Effects of different concentrations of VGB3 (1-200 ng/ml) were evaluated on the viability of HUVEC cells using MTT assay. In addition, downstream signaling pathways in HUVE cells were evaluated through quantitative assessment of protein expression via western blotting.
Results: The results demonstrated that VGB3 treatment inhibited the growth of HUVEC cells. Moreover, Bcl-2 was decreased in the cells treated with the VGB3 compared to the control. Furthermore, VGB3 significantly enhanced the cleaved-caspase7 levels, which is an indicator of apoptosis progression. Altogether, VGB3 enhanced apoptosis in HUVEC cells.
Conclusion: Our results indicate that the peptide might be a potential candidate for antitumor therapy via inhibiting the NF-κB pathway.
