Aralia taibaiensis Protects against I/R-Induced Brain Cell Injury through the Akt/SIRT1/FOXO3a Pathway
| العنوان: | Aralia taibaiensis Protects against I/R-Induced Brain Cell Injury through the Akt/SIRT1/FOXO3a Pathway |
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| المؤلفون: | Jia Cui, Miaomiao Xi, Guo Chao, Yan Weng, Jialin Duan, Aidong Wen, Ying Yin, Hongnan Zheng, Boling Qiao, Jinyi Cao, Yanhua Wang, Guo Wei |
| المصدر: | Oxidative Medicine and Cellular Longevity Oxidative Medicine and Cellular Longevity, Vol 2019 (2019) |
| بيانات النشر: | Hindawi Limited, 2019. |
| سنة النشر: | 2019 |
| مصطلحات موضوعية: | Aging, Article Subject, lcsh:Cytology, Chemistry, Cell Biology, General Medicine, Transfection, Pharmacology, medicine.disease_cause, Biochemistry, In vitro, Blot, In vivo, Apoptosis, medicine, Phosphorylation, lcsh:QH573-671, Protein kinase B, Oxidative stress, Research Article |
| الوصف: | Background. Saponin from Aralia taibaiensis (sAT) showed excellent antioxidative effects in several models; however, its effects on brain cells were unknown to us. The present study was designed to evaluate the protective effects of sAT on ischemia/reperfusion- (I/R-) induced injury and clarify its mechanisms. Methods. In vitro, HT22 cells were pretreated with sAT and then subjected to I/R. Apoptosis rate, mitochondrial function, and antioxidant proteins were measured. To clarify the mechanisms, siRNA were used. In vivo, sAT was pretreated through intragastric administration for 7 days and the I/R model was induced. The neurobehavioral scores, infarction volumes, and some cytokines in the brain were measured. Protein levels were investigated by Western blotting. Results. The results showed that sAT treatment significantly protected cells from I/R-induced cell apoptosis and mitochondrial dysfunction. The antioxidant protein levels were increased in a dose-dependent manner. Further study revealed that sAT induced the deacetylation and phosphorylation of PGC-1α and FOXO3a. sAT treatment also induced the phosphorylation levels of Akt and the expression levels of SIRT1. Using the specific targeted siRNA transfection, the interplay relationship between Akt, SIRT1, PGC-1α, and FOXO3a was verified. Furthermore, the same protective effects were also observed in rats subjected to I/R. Conclusion. sAT protected brain cells from I/R-induced mitochondrial oxidative stress and dysfunction through regulating the Akt/SIRT1/FOXO3a/PGC-1α pathway. |
| وصف الملف: | text/xhtml |
| تدمد: | 1942-0994 1942-0900 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1da72e23c5e9c37faa1c85bc5bc1a1e9 https://doi.org/10.1155/2019/7609765 |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....1da72e23c5e9c37faa1c85bc5bc1a1e9 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 19420994 19420900 |
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