Abstract Title:

Alpha-lipoic acid protects mice against concanavalin A-induced hepatitis by modulating cytokine secretion and reducing reactive oxygen species generation.

Abstract Source:

Int Immunopharmacol. 2016 Mar 25 ;35:53-60. Epub 2016 Mar 25. PMID: 27018751

Abstract Author(s):

Miaomiao Fei, Qun Xie, Yun Zou, Rong He, Yan Zhang, Jun Wang, Lulong Bo, Jinbao Li, Xiaoming Deng

Article Affiliation:

Miaomiao Fei

Abstract:

BACKGROUND: Alpha-lipoic acid (α-LA), which exits in almost all types of prokaryotic and eukaryotic cells, is a key regulator of energy metabolism in mitochondria. This study was designed to explore the protective effect of α-LA against concanavalin A (Con A)-induced hepatitis in mice and explore the potential mechanism.

METHODS: Acute autoimmune hepatitis was induced by intravenous (IV) injection of Con A (15mg/kg) in C57BL/6 mice.α-LA (100mg/kg) was administered four days before Con A injection. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and histopathological change of the liver tissue were measured. Serum cytokine TNF-α, IL-6, IFN-γ and IL-10 were detected by ELISA. The mRNA levels of theseinflammatory cytokines in the liver were detected by RT-PCR. Malondialdehyde (MDA), myeloperoxidase (MPO), superoxide dismutase (SOD) and reduced/oxidized glutathione (GSH/GSSG) in liver were determined using commercial kits. Phosphorylated NF-κB p65, IκBα and phosphorylated MAPK were measured by Western blot.

RESULTS: Con A injection induced severe immune responses and extensive hepatocellular apoptosis within 12h. Pretreatment ofα-LA markedly reduced the serum ALT and AST activity and the increase of plasma TNF-α, IL-6, IFN-γ and IL-10. In addition, α-LA pretreatment decreased the tissue MPO activity and lipid peroxidation, but increased SOD and GSH levels. α-LA inhibited the phosphorylation of NF-κB p65, IκBα and JNK.

CONCLUSION: Pretreatment ofα-LA markedly attenuated Con A-induced hepatitis by modulating cytokine secretion and reducing reactive oxygen species generation.

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