Mechanism of Allicin for Improvement of Hepatic Fibrosis by Regulating Autophagy

Abstract:

Objectives: To explore the effects of allicin on the expression of mitochondrial autophagyrelated proteins in liver tissues of hepatic fibrosis (HF) rats. Materials and Methods: 45 SD rats were randomly divided into Normal, Model, Low, Middle and High groups. The HF rat model was replicated intraperitoneal injection of carbon tetrachloride and ethanol gavage for 4 weeks. Detection of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in rat serum; HE and Masson staining to observe pathological changes; Evaluating LC 3B protein expression by Immunofluorescence; Western Blotting and qRT-PCR methods were used to detect PINK1, Parkin, Beclin 1, and LC3 gene and protein expression levels in rat liver tissues. Results: Compared with the Normal group, the degree of HF in the model group was obvious, the volume fraction of collagen increased significantly (p<0.001), the LC 3B protein expression significantly upregulation (p<0.001), and the rat serum ALT and AST increased significantly (p<0.001, respectively). Up-regulation of PINK1, Parkin, Beclin 1, and LC 3B mRNA and protein expression and LC 3II/LC 3I ratio in liver tissues (p<0.001, respectively); Compared with the model group, Allicin treated groups had reduced HF degree, collagen volume fraction decreased significantly (p<0.05, respectively), LC 3B protein was significantly reduced (p<0.05, respectively), and liver tissue PINK1, Parkin, Beclin 1, and LC3B mRNA and protein expressions, and LC 3II/LC 3I ratio were down-regulated (p<0.05, respectively). Conclusion:Allicin could improve hepatic fibrosis. The mechanism might be related to down-regulating the expression of PINK1, Parkin, Beclin 1, and LC 3 gene and proteins and interfering with the level of mitochondrial autophagy

Keywords: Allicin, HF, PINK1, Parkin, Autophagy.