Chinese Journal of Clinical Anatomy ›› 2021, Vol. 39 ›› Issue (4): 426-430.doi: 10.13418/j.issn.1001-165x.2021.04.012

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Effects of hydrogen sulfide on the autophagy and apoptosis induced by oxygen-glucose deprivation-reoxygenation in rat neuron

Jiang Wenwu1,2, Hong Yue3, Wu Lixiang2, Deng Lvhong4   

  1. 1. Department of Neurological Surgery, the Fifth Affiliated Hospital of Southern Medical University, Guangzhou, 510920, China; 2. Department of Physiology, School of Basic Medicine, Central South University, Changsha 410013, China;  3. Department of Neurological Surgery, the First Affiliated Hospital of University of South China, Hengyang 421001, China;  4. Department of Ophthalmology, the Fifth Affiliated Hospital of Southern Medical University, Guangzhou 510920, China
  • Received:2020-04-05 Online:2021-07-25 Published:2021-07-25

Abstract: Objective To investigate the effects of exogenous hydrogen sulfide (H2S) on autophagy and injury induced by oxygen glucose deprivation/reoxygenation (OGD/R) in neurons, and to clarify the molecular mechanism of H2S attenuating cerebral ischemia-reperfusion injury in rats. Methods Rat neuronal PC12 cells were used as the research object. Classical OGD/R was used to induce cell damage. Sodium thiosulfate (NaHS), a donor of H2S, was used to observe the effect of H2S on OGD/R-induced mTOR, AMPK and its phosphorylated AMPK. In order to clarify the role of AMPK in the regulation of autophagy in PC12 cells by H2S, AMPK overexpression plasmid was used to observe the effect of H2S on the damage of PC12 cells. Results The OGD/R-treated PC12 cells had decreased mTOR phosphorylation level and enhanced AMPK activity, and NaHS pretreatment partially reversed the above changes. The overexpression of AMPK can abolish the inhibitory effect of NaHS on OGD/R-induced autophagy and cell damage. Conclusions H2S can inhibit the autophagy of brain neurons during ischemia-reperfusion by inhibiting the activation of AMPK, and finally reduce neuronal damage.

Key words:  , Hydrogen sulfide, Autophagy,  Oxygen-glucose deprivation-reoxygenation,  Sodium hydrosulfide

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