scholarly journals Cistanches deserticola PhG-RE through Inhibiting ERS Apoptosis Mechanism to Protect Myocardial Cell Apoptosis from H2O2-Induced Endoplasmic Reticulum Stress

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Tianwei Lan ◽  
Qian Yu
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cell Apoptosis ◽  
Cell Damage ◽  
Damage Model ◽  
Myocardial Cell ◽  
Protective Effects ◽  
Myocardial Cells ◽  
Caspase 12 ◽  
Apoptotic Factors

The herb Cistanche deserticola has some myocardial protective effects. This study attempted to explain the mechanism by which PhG-RE protects myocardial cells and verify if this protection occurs through regulating the apoptosis mechanism associated with endoplasmic reticulum stress (ERS). Rat myocardial cells were exposed to 150 μg·mL−1 PhG-RE for 24 h and then to 100 μmol·mL−1 H2O2 for 18 h to induce ERS and establish a cell damage model. Thapsigargin (TG), a specific ERS activator, and 4-phenylbutyric acid (4-PBA), an ERS inhibitor, were used to validate the accuracy of the experiment. Our results demonstrated that PhG-RE significantly improved cell viability, protected cells, and reduced cell damage and apoptosis. PhG-RE played a role similar to that of the ERS inhibitor 4-PBA in protecting myocardial cells against apoptosis and damage induced by ER stress. Furthermore, PhG-RE significantly attenuated the mRNA expression of the ERS-associated apoptotic factors GRP78, CHOP, and Caspase-12 and the protein expression of the ERS-associated apoptotic factors GRP78, CHOP, Caspase-12, and p-JNK. Taken together, these findings suggest that PhG-RE can effectively protect myocardial cells and reduce cell apoptosis and damage, which may be related to the regulation of ERS-associated apoptosis.

scholarly journals High Doses of Dexamethasone Induce Endoplasmic Reticulum Stress-Mediated Apoptosis by Promoting Calcium Ion Influx-Dependent CHOP Expression in Osteoblasts

2021 ◽  
Author(s):  
Yunshan Guo ◽  
Dingjun Hao
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cell Apoptosis ◽  
Calcium Ion ◽  
Caspase 3 ◽  
Combined Treatment ◽  
Caspase 12 ◽  
Ion Influx ◽  
High Doses ◽  
In Cells

Abstract Background: The molecular mechanisms by which dexamethasone (Dex) induces apoptosis in osteoblasts remain unclear.Materials and Methods: MC3T3-E1 cells were treated with 0, 10-8, 10-6, and 10-4 M Dex for 24 h. The expression of ATF6, and phosphorylated PERK and IRE1, cell apoptosis, and the activity of caspase-12 and caspase-3 were measured. The expression of CHOP and the rate of influx of calcium ions were also measured in cells treated with 0 and 10-4 M Dex for 24 h. The effect of 2-APB treatment was assessed in cells treated with 0 or 10-4 M Dex.Results: The levels of ATF6 and phosphorylated PERK and IRE1 increased in a dose-dependent manner in MC3T3-E1 cells treated with 10-8, 10-6, and 10-4 M Dex, compared to in cells treated with 0 M Dex (P <0.05). Cells treated with 10-6 and 10-4 M Dex had significantly increased cell apoptosis rates and caspase-12 and caspase-3 activity compared to the control (P <0.05). Cells treated with 10-4 M Dex had significantly increased levels of CHOP and calcium ion influx rates compared to in the control (P <0.05). Combined treatment with 10-4 M Dex and 2-APB abrogated the observed increases in cell apoptosis and the activity of caspase-12 and caspase-3 (P>0.05). Conclusion: High doses of Dex induce endoplasmic reticulum stress-mediated apoptosis by promoting calcium ion influx-dependent expression of CHOP, and the activation of caspase-12 and caspase-3 in osteoblasts. Combined treatment with 2-APB protects the cells from the effects of Dex, preventing endoplasmic reticulum stress-mediated apoptosis.

scholarly journals Hesperidin Protects against Acute Alcoholic Injury through Improving Lipid Metabolism and Cell Damage in Zebrafish Larvae

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Zhenting Zhou ◽  
Weichao Zhong ◽  
Haiyan Lin ◽  
Peng Huang ◽  
Ning Ma ◽  
...  
Keyword(s):  
Dna Damage ◽  
Endoplasmic Reticulum ◽  
Lipid Metabolism ◽  
Endoplasmic Reticulum Stress ◽  
Cell Damage ◽  
Animal Experiments ◽  
Major Constituent ◽  
Egfp Expression ◽  
Protective Effects ◽  
Zebrafish Larvae

Alcoholic liver disease (ALD) is a series of abnormalities of liver function, including alcoholic steatosis, steatohepatitis, and cirrhosis. Hesperidin, the major constituent of flavanone in grapefruit, is proved to play a role in antioxidation, anti-inflammation, and reducing multiple organs damage in various animal experiments. However, the underlying mechanism of resistance to alcoholic liver injury is still unclear. Thus, we aimed to investigate the protective effects of hesperidin against ALD and its molecular mechanism in this study. We established an ALD zebrafish larvae model induced by 350 mM ethanol for 32 hours, using wild-type and transgenic line with liver-specific eGFP expressionTg (lfabp10α:eGFP)zebrafish larvae (4 dpf). The results revealed that hesperidin dramatically reduced the hepatic morphological damage and the expressions of alcohol and lipid metabolism related genes, includingcyp2y3,cyp3a65,hmgcra,hmgcrb,fasn, and fads2compared with ALD model. Moreover, the findings demonstrated that hesperidin alleviated hepatic damage as well, which is reflected by the expressions of endoplasmic reticulum stress and DNA damage related genes (chop,gadd45αa,andedem1). In conclusion, this study revealed that hesperidin can inhibit alcoholic damage to liver of zebrafish larvae by reducing endoplasmic reticulum stress and DNA damage, regulating alcohol and lipid metabolism.

scholarly journals Protective Mechanism of KIOM-4 in Streptozotocin-Induced Pancreatic β-Cells Damage Is Involved in the Inhibition of Endoplasmic Reticulum Stress

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Rui Zhang ◽  
Jin Sook Kim ◽  
Kyoung Ah Kang ◽  
Mei Jing Piao ◽  
Ki Cheon Kim ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Er Stress ◽  
Apoptotic Cell ◽  
Cell Damage ◽  
Initiation Factor ◽  
Protective Mechanism ◽  
Protective Effects ◽  
Initiation Factor 2 ◽  
Activating Transcription Factor

Endoplasmic reticulum stress-mediated apoptosis plays an important role in the destruction of pancreaticβ-cells and contributes to the development of type 1 diabetes. The present study examined the effect of KIOM-4, a mixture of four plant extracts, on streptozotocin- (STZ-) induced endoplasmic reticulum (ER) stress in rat pancreaticβ-cells (RINm5F). KIOM-4 was found to inhibit STZ-induced apoptotic cell death, confirmed by formation of apoptotic bodies and DNA fragmentation. STZ was found to induce the characteristics of ER stress; mitochondrial Ca2+overloading, enhanced ER staining, release of glucose-regulated protein 78 (GRP78), phosphorylation of RNA-dependent protein kinase (PKR) like ER kinase (PERK) and eukaryotic initiation factor-2α(eIF-2α), cleavage of activating transcription factor 6 (ATF6) and caspase 12, and upregulation of CCAAT/enhancer-binding protein-homologous protein (CHOP). However, KIOM-4 attenuated these changes induced by STZ. Furthermore, KIOM-4 suppressed apoptosis induced by STZ in CHOP downregulated cells using CHOP siRNA. These results suggest that KIOM-4 exhibits protective effects in STZ-induced pancreaticβ-cell damage, by interrupting the ER stress-mediated pathway.

scholarly journals hAMSC-CM Attenuates Paraquat-Induced A549 Cell Damage by Reducing Endoplasmic Reticulum Stress and Oxidative Stress

2021 ◽  
Author(s):  
Futuan Liao ◽  
Liming Gong ◽  
Lijing Jia ◽  
Jianhong Wang ◽  
Tongying Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cell Damage ◽  
Intervention Group ◽  
A549 Cells ◽  
Protective Effects ◽  
Stress Oxidative ◽  
Stress Damage ◽  
And Oxidative Stress

Abstract Acute paraquat (PQ) poisoning results in severe acute lung injury and pulmonary fibrosis, and there is no specific antidote; thus, the mortality rate of PQ poisoning is extremely high. The mechanism of poisoning may be associated with endoplasmic reticulum stress, oxidative stress damage and organ/tissue inflammation. Recent studies have reported that human amnion-derived mesenchymal stem cells (hAMSCs) secrete a variety of cytokines, and that hAMSC-conditioned medium (CM) has anti-inflammatory and immunomodulatory effects. The aim of the present study was to investigate whether hAMSC-CM exerts protective effects against PQ toxicity in A549 cells. The data demonstrated that the activity of A549 cells was decreased after 24 h of PQ exposure and that the cell viability of the hAMSC-CM intervention group was higher compared with the PQ-only group. hAMSC-CM intervention decreased cell damage, apoptosis rates, oxidative stress indexes, Bax/Bcl-2 ratios and CHOP expression levels in poisoned cells by CCK-8 experiment, apoptosis detection, ROS content detection, and Western blot analysis respectively. In conclusion, hAMSC-CM may attenuate the cell damage caused by PQ by reducing endoplasmic reticulum stress and oxidative stress.

Sign in / Sign up

Export Citation Format

Share Document