Upregulation of DAPK2 ameliorates oxidative damage and apoptosis of placental cells in hypertensive disorder complicating pregnancy by suppressing human placental microvascular endothelial cell autophagy through the mTOR signaling pathway

2019 ◽  
Vol 121 ◽  
pp. 488-497 ◽  
Author(s):  
Yan Wang ◽  
Lian-Lian Liu ◽  
Yuan Tian ◽  
Yang Chen ◽  
Wen-Hui Zha ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Oxidative Damage ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Microvascular Endothelial Cell ◽  
Hypertensive Disorder ◽  
Mtor Signaling Pathway ◽  
Hypertensive Disorder Complicating Pregnancy ◽  
Placental Cells ◽  
Microvascular Endothelial

scholarly journals Autophagy protects gastric mucosal epithelial cells from ethanol-induced oxidative damage via mTOR signaling pathway

2017 ◽  
Vol 242 (10) ◽  
pp. 1025-1033 ◽  
Author(s):  
Weilong Chang ◽  
Jie Bai ◽  
Shaobo Tian ◽  
Muyuan Ma ◽  
Wei Li ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Epithelial Cells ◽  
Oxidative Damage ◽  
Signaling Pathway ◽  
Cell Damage ◽  
Mtor Signaling ◽  
Adaptive Mechanism ◽  
Mtor Signaling Pathway ◽  
Mucosal Epithelial Cell ◽  
Ethanol Toxicity

Alcohol abuse is an important cause of gastric mucosal epithelial cell injury and gastric ulcers. A number of studies have demonstrated that autophagy, an evolutionarily conserved cellular mechanism, has a protective effect on cell survival. However, it is not known whether autophagy can protect gastric mucosal epithelial cells against the toxic effects of ethanol. In the present study, gastric mucosal epithelial cells (GES-1 cells) and Wistar rats were treated with ethanol to detect the adaptive response of autophagy. Our results demonstrated that ethanol exposure induced gastric mucosal epithelial cell damage, which was accompanied by the downregulation of mTOR signaling pathway and activation of autophagy. Suppression of autophagy with pharmacological agents resulted in a significant increase of GES-1 cell apoptosis and gastric mucosa injury, suggesting that autophagy could protect cells from ethanol toxicity. Furthermore, we evaluated the cellular oxidative stress response following ethanol treatment and found that autophagy induced by ethanol inhibited generation of reactive oxygen species and degradation of antioxidant and lipid peroxidation. In conclusion, these findings provide evidence that ethanol can activate autophagy via downregulation of the mTOR signaling pathway, serving as an adaptive mechanism to ameliorate oxidative damage induced by ethanol in gastric mucosal epithelial cells. Therefore, modifying autophagy may provide a therapeutic strategy against alcoholic gastric mucosa injury. Impact statement The effect and mechanism of autophagy on ethanol-induced cell damage remain controversial. In this manuscript, we report the results of our study demonstrating that autophagy can protect gastric mucosal epithelial cells against ethanol toxicity in vitro and in vivo. We have shown that ethanol can activate autophagy via downregulation of the mTOR signaling pathway, serving as an adaptive mechanism to ameliorate ethanol-induced oxidative damage in gastric mucosal epithelial cells. This study brings new and important insights into the mechanism of alcoholic gastric mucosal injury and may provide an avenue for future therapeutic strategies.

Kaempferol reversals retinal ischemia/reperfusion (IR) injury through activating of PI3K/Akt/mTOR signaling pathway

2021 ◽  
Author(s):  
Da Sun ◽  
Fusheng Shang ◽  
Dagui Chen ◽  
Wenwen Wang ◽  
lili lin
Keyword(s):  
Oxidative Damage ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Ischemia Reperfusion ◽  
Retinal Ischemia ◽  
Mtor Signaling ◽  
Cell Counting ◽  
Mtor Signaling Pathway ◽  
Autophagy Gene ◽  
Retinal Vascular Occlusion

Abstract Purpose Retinal ischemia/reperfusion (IR) injury is associated with many ocular diseases, including acute glaucoma, diabetic retinopathy, and retinal vascular occlusion. However, currently there are no effective medications to prevent the development ofretinal IR injury.Kaempferol is a kind of plant extract which has showed an excellent ability to inhibit the inflammation.. Materials and Methods In this study, both in vitro and in vivo retinaloxidative damage models were established.Cell viability was assessed by Cell Counting Kit-8 assay. Apoptosis was examined using flow cytometry analysis.Atherosclerotic lesion analysis was performed using hematoxylin-eosin staining,The expressions of Inflammatory cytokines were detected by quantitative real-time PCR and ELISA respectively.The effect of expression of apoptosis、utophagy and the PI3K/Akt/mTOR signaling pathway related pathway was evaluated by Western blot. Results We found kaempferol was able to protect the viability of ARPE-19 cells against oxidative damage by reducing its apoptosis. In addition, it also kept structurally complete epithelium, stroma and endothelium of cornea after oxidative damage. Moreover, it also able to reduce the expression of inflammatory cytokines and increased the expression of anti-inflammatory cytokines.Kaempferol was able to enhanced the expression of anti-apoptotic genes BCL-2, and reduced the expression of autophagy gene Beclin 1 and increased the expression of anti-autophagy gene LC-3,was also able to enhance the expression PI3K and the phosphorylation ofAkt andmTOR. Conclusion Kaempferolreversals retinal ischemia/reperfusion (IR) injury through activating of PI3K/Akt/mTOR signaling pathway.

scholarly journals Autophagy Induced by ROS Aggravates Testis Oxidative Damage in Diabetes via Breaking the Feedforward Loop Linking p62 and Nrf2

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Yuanyuan Tian ◽  
Wei Song ◽  
Dongsheng Xu ◽  
Xiao Chen ◽  
Xiaojiao Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Male Infertility ◽  
Oxidative Damage ◽  
Signaling Pathway ◽  
Practical Method ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Feedforward Loop ◽  
Testicular Dysfunction

Testicular dysfunction due to hyperglycemia is the main cause of infertility in diabetic men. Over the years, in order to solve this growing problem, a lot of research has been done and a variety of treatments have been created, but so far, there is no safe, effective, and practical method to prevent male infertility caused by diabetes. In this review, we emphasize the male infertility mechanism caused by diabetes from the effects of oxidative stress and autophagy on the function of testes via the PI3K/Akt/mTOR signaling pathway, and we highlight that oxidative stress-induced autophagy breaks the feedforward loop linking Nrf2 and p62 and promotes oxidative damage in diabetic testes.

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