Protective effects of Elaeagnus angustifolia L. leaves against H2O2-induced oxidative damage in Rat Schwann Cells (RSC-96) through regulation of PI3K/Akt signaling pathway

2021 ◽  
Vol 17 (74) ◽  
pp. 315
Author(s):  
Han-Lin Xu ◽  
Yun Sun ◽  
Hui Yao ◽  
Xin Zhang ◽  
Xiao-Xuan Yuan
Keyword(s):  
Oxidative Damage ◽  
Signaling Pathway ◽  
Schwann Cells ◽  
Akt Signaling ◽  
Protective Effects ◽  
Elaeagnus Angustifolia ◽  
Akt Signaling Pathway

scholarly journals The Antagonistic Effect of Glutamine on Zearalenone-Induced Apoptosis via PI3K/Akt Signaling Pathway in IPEC-J2 Cells

Toxins ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 891
Author(s):  
Tianhu Wang ◽  
Jingjing Wang ◽  
Tong Zhang ◽  
Aixin Gu ◽  
Jianping Li ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Signaling Pathway ◽  
Nuclear Fission ◽  
Akt Signaling ◽  
Antagonistic Effect ◽  
Protective Effects ◽  
Akt Signaling Pathway ◽  
Pi3k Inhibitor Ly294002 ◽  
Apoptotic Genes ◽  
Induced Apoptosis

Zearalenone (ZEN) is a non-steroidal estrogen mycotoxin produced by Fusarium fungi, which inevitably exists in human and animal food or feed. Previous studies indicated that apoptosis seems to be a key determinant of ZEN-induced toxicity. This experiment aimed to investigate the protective effects of Glutamine (Gln) on ZEN-induced cytotoxicity in IPEC-J2 cells. The experimental results showed that Gln was able to alleviate the decline of cell viability and reduce the production of reactive oxygen species and calcium (Ca2+) induced by ZEN. Meanwhile, the mRNA expression of antioxidant enzymes such as glutathione reductase, glutathione peroxidase, and catalase was up-regulated after Gln addition. Subsequently, Gln supplementation resulted in the nuclear fission and Bad-fluorescence distribution of apoptotic cells were weakened, and the mRNA expression and protein expression of pro-apoptotic genes and apoptotic rates were significantly reduced. Moreover, ZEN reduced the phosphorylation Akt, decreased the expression of Bcl-2, and increased the expression of Bax. Gln alleviated the above changes induced by ZEN and the antagonistic effects of Gln were disturbed by PI3K inhibitor (LY294002). To conclude, this study revealed that Gln exhibited significant protective effects on ZEN-induced apoptosis, and this effect may be attributed to the PI3K/Akt signaling pathway.

413-P: SIRT1 Overexpression Restores the Protective Effects of Ischemic Post-conditioning in Diabetic Mice via Modulating Akt Signaling Pathway

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 413-P
Author(s):  
MINGGE DING ◽  
KE ZENG ◽  
MINGZHE YU ◽  
CHAOYANG LIU ◽  
FENG FU
Keyword(s):  
Signaling Pathway ◽  
Akt Signaling ◽  
Protective Effects ◽  
Diabetic Mice ◽  
Akt Signaling Pathway

Netrin-1 induces the migration of Schwann cells via p38 MAPK and PI3K-Akt signaling pathway mediated by the UNC5B receptor

2015 ◽  
Vol 464 (1) ◽  
pp. 263-268 ◽  
Author(s):  
Jianwei Lv ◽  
Xiaolei Sun ◽  
Jianxiong Ma ◽  
Xinlong Ma ◽  
Yang Zhang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Schwann Cells ◽  
P38 Mapk ◽  
Akt Signaling ◽  
Akt Signaling Pathway

scholarly journals Asiatic Acid Protects against Doxorubicin-Induced Cardiotoxicity in Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Xiaoping Hu ◽  
Baijun Li ◽  
Luocheng Li ◽  
Bowen Li ◽  
Jinlong Luo ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Signaling Pathway ◽  
Cardiac Injury ◽  
Akt Signaling ◽  
Cardiac Complications ◽  
Asiatic Acid ◽  
Protective Effects ◽  
Akt Signaling Pathway ◽  
Myocardial Oxidative Stress

The use of doxorubicin (DOX) can result in depression of cardiac function and refractory cardiomyopathy. Currently, there are no effective approaches to prevent DOX-related cardiac complications. Asiatic acid (AA) has been reported to provide cardioprotection against several cardiovascular diseases. However, whether AA could attenuate DOX-related cardiac injury remains unclear. DOX (15 mg/kg) was injected intraperitoneally into the mice to mimic acute cardiac injury, and the mice were given AA (10 mg/kg or 30 mg/kg) for 2 weeks for protection. The data in our study found that AA-treated mice exhibited attenuated cardiac injury and improved cardiac function in response to DOX injection. AA also suppressed myocardial oxidative damage and apoptosis without affecting cardiac inflammation in DOX-treated mice. AA also provided protection in DOX-challenged cardiomyocytes, improved cell viability, and suppressed intracellular reactive oxygen species (ROS) in vitro. Detection of signaling pathways showed that AA activated protein kinase B (AKT) signaling pathway in vivo and in vitro. Furthermore, we found that AA lost its protective effects in the heart with AKT inactivation. In conclusion, our results found that AA could attenuate DOX-induced myocardial oxidative stress and apoptosis via activation of the AKT signaling pathway.

scholarly journals Chrysanthemum indicum Prevents Hydrogen Peroxide-Induced Neurotoxicity by Activating the TrkB/Akt Signaling Pathway in Hippocampal Neuronal Cells

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 3690
Author(s):  
Yun Hee Jeong ◽  
Tae In Kim ◽  
You-Chang Oh ◽  
Jin Yeul Ma
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Oxidative Damage ◽  
Neurodegenerative Diseases ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Ht22 Cells ◽  
Chrysanthemum Indicum ◽  
Antioxidant Effects

Oxidative stress-mediated neuronal damage is associated with the pathogenesis and development of neurodegenerative diseases. Chrysanthemum indicum has antioxidant properties. However, the neuroprotective effects and the cellular mechanism of C. indicum ethanol extract (CIE) against oxidative damage in hippocampal neuronal cells have not been clearly elucidated. Therefore, this study investigated whether CIE has protective effects against hydrogen peroxide (H2O2)-induced oxidative toxicity in HT22 cells. CIE pretreatment significantly improved neuronal cell viability. Moreover, the formation of intracellular reactive oxygen species and apoptotic bodies, and mitochondrial depolarization were significantly reduced in HT22 cells with H2O2-induced oxidative toxicity. Furthermore, CIE increased the phosphorylation of tropomyosin-related kinase receptor B (TrkB), protein kinase B (Akt), cAMP response element-binding protein, the expression of brain-derived neurotrophic factor, antioxidant enzymes, and the nuclear translocation of nuclear factor erythroid 2-related factor 2 by activating the TrkB/Akt signaling pathway. In contrast, the addition of K252a, a TrkB inhibitor, or MK-2206, an Akt-selective inhibitor, reduced the neuroprotective and antioxidant effects of CIE. Taken together; CIE exhibits neuroprotective and antioxidant effects against oxidative damage. Therefore, it can be a potential agent for treating oxidative stress-related neurodegenerative diseases.

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