Cheng Ping, Chen Kan, Xia Yujing, Dai Weiqi, Wang Fan, Shen Miao, Wang Chengfen, Yang Jing, Zhu Rong, Zhang Huawei, Li Jingjing, Zheng Yuanyuan, Wang Junshan, Zhang Yan, Lu Jie, Zhou Yingqun, Guo Chuanyong
Department of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University of Medicine, Shanghai, People's Republic of China.
Drug Des Devel Ther. 2014 Sep 9;8:1277-86. doi: 10.2147/DDDT.S66573. eCollection 2014.
Hydrogen sulfide (H2S) is known to exert anti-inflammatory properties. Apoptosis and autophagy play important roles in concanavalin A (Con A)-induced acute hepatitis. The purpose of this study was to explore both the effect and mechanism of H2S on Con A-induced acute hepatitis.
BALB/c mice were randomized into sham group, Con A-injection group, and 14 μmol/kg of sodium hydrosulfide (NaHS, an H2S donor) pretreatment group.
Aspartate aminotransferase, alanine aminotransferase, and pathological damage were significantly ameliorated by NaHS pretreatment. NaHS pretreatment significantly reduced the levels of interleukin-6 and tumor necrosis factor-α compared with those of the Con A group. The expression of Bcl-2, Bax, Beclin-1, and LC3-2, which play important roles in the apoptosis and autophagy pathways, were also clearly affected by NaHS. Furthermore, NaHS affected the p-mTOR and p-AKT.
H2S attenuates Con A-induced acute hepatitis by inhibiting apoptosis and autophagy, in part, through activation of the PtdIns3K-AKT1 signaling pathway.
已知硫化氢（H₂S）具有抗炎特性。凋亡和自噬在刀豆蛋白A（Con A）诱导的急性肝炎中起重要作用。本研究的目的是探讨H₂S对Con A诱导的急性肝炎的作用及其机制。
将BALB/c小鼠随机分为假手术组、Con A注射组和14 μmol/kg硫氢化钠（NaHS，一种H₂S供体）预处理组。
NaHS预处理可显著改善天冬氨酸转氨酶、丙氨酸转氨酶水平及病理损伤。与Con A组相比，NaHS预处理显著降低了白细胞介素-6和肿瘤坏死因子-α的水平。在凋亡和自噬途径中起重要作用的Bcl-2、Bax、Beclin-1和LC3-2的表达也受到NaHS的明显影响。此外，NaHS影响p-mTOR和p-AKT。
H₂S通过部分激活磷脂酰肌醇3激酶-AKT1信号通路抑制凋亡和自噬，从而减轻Con A诱导的急性肝炎。
