Department of Gastroenterology, Shantou Central Hospital, Affiliated Hospital of Sun Yat-Sen University, Shantou, Guangdong province, China.
Department of Endocrine and Metabolic Diseases, 1st Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong province, China.
Ann Hepatol. 2018 May-June;17(3):511-518. doi: 10.5604/01.3001.0011.7396. Epub 2018 Apr 9.
Hepatitis C virus core-binding protein 6 (HCBP6) was previously found to be an hepatitis C virus corebinding protein, its biological function remains unclear. Our research aims to investigate the role of HCBP6 in the development of hepatic steatosis induced by high-fat diet and carbon tetrachloride (CCL4) in rats.
Eighteen Wistar rats were randomly allocated into 3 groups: control group, model group 1, and model group 2. The control group was treated with a standard diet for 5 weeks. Model groups were treated with high-fat diet and CCL4 injection twice a week for 3 weeks in Group 1 and 5 weeks in Group 2, respectively. After the intervention, hepatic steatosis was observed by histological staining with hematoxylin and eosin (H&E) and Oil Red O staining. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total colesterol (TC), and triglycerides (TGs) were measured. The TG content in liver homogenates was evaluated. Expressions of HCBP6 and SREBP-1c were determined by immunofluorescence, quantitative real-time PCR, and Western blot analysis.
Hepatic steatosis was successfully induced in model groups. ALT, AST, TC, and TGs elevated in model groups compared with those in control group (P < 0.05). Hepatic steatosis induced by high-fat diet and CCL4 resulted in low expression of HCBP6 and high expression of SREBP-1c in the liver of rats (P < 0.05).
HCBP6 is involved in the development of high-fat diet- and CCL4-induced hepatic steatosis and related negatively with SREBP-1c.
丙型肝炎病毒核心结合蛋白 6(HCBP6)先前被发现是一种丙型肝炎病毒核心结合蛋白,但其生物学功能尚不清楚。我们的研究旨在探讨 HCBP6 在高脂肪饮食和四氯化碳(CCL4)诱导大鼠肝脂肪变性发展中的作用。
将 18 只 Wistar 大鼠随机分为 3 组:对照组、模型组 1 组和模型组 2 组。对照组给予标准饮食 5 周。模型组 1 组给予高脂肪饮食和 CCL4 注射,每周 2 次,共 3 周;模型组 2 组给予高脂肪饮食和 CCL4 注射,每周 2 次,共 5 周。干预结束后,通过苏木精和伊红(H&E)染色和油红 O 染色观察肝脂肪变性。检测血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、总胆固醇(TC)和甘油三酯(TGs)水平。评估肝匀浆中 TG 含量。通过免疫荧光、实时定量 PCR 和 Western blot 分析检测 HCBP6 和 SREBP-1c 的表达。
模型组成功诱导肝脂肪变性。与对照组相比,模型组 ALT、AST、TC 和 TGs 升高(P < 0.05)。高脂肪饮食和 CCL4 诱导的肝脂肪变性导致大鼠肝脏中 HCBP6 表达降低,SREBP-1c 表达升高(P < 0.05)。
HCBP6 参与了高脂肪饮食和 CCL4 诱导的肝脂肪变性的发生发展,与 SREBP-1c 呈负相关。