Journal of Capital Medical University ›› 2015, Vol. 36 ›› Issue (1): 116-120.doi: 10.3969/j.issn.1006-7795.2015.01.022

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Effects of exogenous hydrogen sulfide on autophagy of HepG2 cells

Chen Ning1, Wang Shanshan2, Chen Yuhan1, Yin Jiming2, Chen Dexi2, Ding Huiguo1   

  1. 1. Department of Gastroenterology and Hepatology, Beijing You'an Hospital, Capital Medical University, Beijing 100069, China;
    2. Beijing Institute of Hepatology, Beijing 100069, China
  • Received:2014-11-21 Online:2015-02-21 Published:2015-01-31
  • Supported by:
    This study was supported by National Natural Science Foundation of China (3087225); Beijing Municipal Science and Technology Project(Z111107058811067); Beijing High-Level Talent Academic Leader/Personnel Training Programs awarded to Ding HG (2011-2-19).

Abstract: Objective To investigate the effects of exogenous hydrogen sulfide (H2S) on the autophagy of HepG2 cells and its underlying mechanism.Methods HepG2 cells were administrated by sodium hydrosulfide (NaHS), a donor of H2S, for 24h, the expression of autophagy-related protein LC3-Ⅱ was detected via Western blotting; The mRNA level of autophagy related gene beclin1 and atg5 were detected via RT-PCR. The autophagy particles and apoptosis were observed using immunofluorescence. AnnexinV/PI flow cytometry were performed to assess the effect of NaHS on cell apoptosis. Results NaHS enhanced the autophagy-related protein (LC3-Ⅱ) expression and beclin1 mRNA, atg5 mRNA and autophagosome formation compared with control. 3-MA could inhibit NaHS-induced autophagy.Immunofluorescence showed the M30 positive cells were significantly increased compared with the controls.Additionally, both the nuclear heterochromatin and apoptotic bodies were significantly increased. Flowcytometry showed that NaHS increased the apoptosis rate of HepG2 cells. Conclusion The autophagy is induced by exogenous hydrogen sulfide through the autophagy related genes (beclin1 and atg5), and can promote apoptosis in HepG2 cells.

Key words: hydrogen sulfide, autophagy, microtubule-associated light chain 3-Ⅱ(LC3-Ⅱ), apoptosis

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