Article Publish Status: FREE
Abstract Title:

Eugenol Attenuates Cerebral Ischemia-Reperfusion Injury by Enhancing AutophagyAMPK-mTOR-P70S6K Pathway.

Abstract Source:

Front Pharmacol. 2020 ;11:84. Epub 2020 Feb 21. PMID: 32153404

Abstract Author(s):

Xiaowei Sun, Dongyan Wang, Tingting Zhang, Xuejian Lu, Fangfang Duan, Lili Ju, Xiaotong Zhuang, Xicheng Jiang

Article Affiliation:

Xiaowei Sun


Eugenol, as an active compound isolated from Acorus gramineus, has been shown to protect against cerebral ischemia-reperfusion (I/R) injury. Nonetheless, the detailed neuroprotective mechanisms of eugenol in cerebral I/R injury have not been elaborated. In the present study, cerebral I/R injury model was established by middle cerebral artery occlusion (MCAO) in rats. HT22 cells were subjected to oxygen-glucose deprivation/reperfusion (OGD/R) to mimic cerebral I/R injury. The results showed that eugenol pre-treatment relieved cerebral I/R injury as evidenced by improving neurological deficits and reducing infarct volume. Autophagy was induced by MCAO, which was further promoted by eugenol administration. Moreover, rapamycin, an activator of autophagy, promoted eugenol-induced decreases in neurological score, infarct volume, brain water content, and apoptosis. However, pretreatment with 3-MA, an inhibitor of autophagy, led to the opposite results. Similarly, eugenol pretreatment increased the viability and restrained apoptosis of OGD/R-challenged HT22 cells. OGD/R-induced autophagy was strengthened by eugenol. Mechanically, eugenol promoted autophagy through regulating AMPK/mTOR/P70S6K signaling pathwayand. In conclusion, pretreatment with eugenol attenuated cerebral I/R injury by inducing autophagyAMPK/mTOR/P70S6K signaling pathway.

Study Type : Animal Study, In Vitro Study

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Sayer Ji
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