scholarly journals Reduction of SIRT1 blunts the protective effects of ischemic post-conditioning in diabetic mice by impairing the Akt signaling pathway

2019 ◽  
Vol 1865 (6) ◽  
pp. 1677-1689
Author(s):  
Mingge Ding ◽  
Lang Hu ◽  
Hongyan Yang ◽  
Chao Gao ◽  
Ke Zeng ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Akt Signaling ◽  
Protective Effects ◽  
Diabetic Mice ◽  
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

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.

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