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Hydrogen sulfide, a potential novel drug, attenuates concanavalin A-induced hepatitis

机译:硫化氢,一种潜在的新药,可减轻伴刀豆球蛋白A引起的肝炎

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Background: 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. Methods: 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. Results: 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. Conclusion: H2S attenuates Con A-induced acute hepatitis by inhibiting apoptosis and autophagy, in part, through activation of the PtdIns3K-AKT1 signaling pathway.
机译:背景:硫化氢(H2S)具有消炎作用。凋亡和自噬在伴刀豆球蛋白A(Con A)诱导的急性肝炎中起重要作用。这项研究的目的是探讨H2S对Con A诱发的急性肝炎的作用及其机制。方法:将BALB / c小鼠随机分为假手术组,Con A注射组和14μmol/ kg的硫化氢钠(NaHS,H2S供体)预处理组。结果:NaHS预处理可显着改善天冬氨酸转氨酶,丙氨酸转氨酶和病理损伤。与Con A组相比,NaHS预处理可显着降低白介素6和肿瘤坏死因子-α的水平。在细胞凋亡和自噬途径中起重要作用的Bcl-2,Bax,Beclin-1和LC3-2的表达也明显受到NaHS的影响。此外,NaHS影响了p-mTOR和p-AKT。结论:H2S通过抑制细胞凋亡和自噬,部分通过PtdIns3K-AKT1信号通路的激活来减轻Con A诱导的急性肝炎。

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