Ningbo Affiliated TCM Hospital of Zhejiang Chinese Medicine University, Zhejiang, China.
Turk J Gastroenterol. 2020 Dec;31(12):902-909. doi: 10.5152/tjg.2020.19568.
BACKGROUND/AIMS: This study aimed to explore the therapeutic effects and underlying mechanism of berberine (BBR) on the non-alcoholic fatty liver disease (NAFLD) induced by high-fat diet (HFD).
Rats were randomly divided into the following 4 groups: control (normal diet), model (HFD), polyene phosphatidylcholine HFD+PPC, and BBR (HFD+BBR) group. The NAFLD models were prepared by feeding with HFD for 12 weeks. The liver tissues were observed by oil red O staining. H-E staining was used to detect pathological changes in the liver tissues. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were detected by an automatic biochemical analyzer. ELISA was performed to observe the inflammatory cytokines (TNF-α, IL-6, and IL-1β) expressions. The levels of TLR4, MyD88, and NF-κB p65 were analyzed using western blot and qRT-PCR, respectively. The nuclear translocation levels of NF-κB in the primary liver cells were measured using flow cytometry.
BBR could significantly alleviate the liver tissue steatosis and inflammatory cell infiltration; reduce the NAFLD activity scores and serum levels of ALT, AST, TC, and LDL-C; decrease the levels of TNF-α, IL-6, and IL-1β, and reduce the expression of TLR4, MyD88, and NF-κB in the liver tissues. BBR could also reverse the nuclear translocation of NF-κB in the primary liver cells.
BBR alleviated the progress of NAFLD and liver damage, which might contribute to inhibit the nuclear translocation of NF-κB via the TLR4/MyD88/NF-κB pathway.
背景/目的：本研究旨在探讨小檗碱（BBR）对高脂肪饮食（HFD）诱导的非酒精性脂肪性肝病（NAFLD）的治疗作用及其机制。
将大鼠随机分为以下 4 组：对照组（正常饮食）、模型组（HFD）、多烯磷脂酰胆碱 HFD+PPC 组和 BBR（HFD+BBR）组。用 HFD 喂养 12 周制备 NAFLD 模型。用油红 O 染色观察肝组织。用 H-E 染色检测肝组织的病理变化。用自动生化分析仪检测血清丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）、总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）和高密度脂蛋白胆固醇（HDL-C）水平。采用 ELISA 法观察炎症细胞因子（TNF-α、IL-6 和 IL-1β）的表达。用 Western blot 和 qRT-PCR 分别分析 TLR4、MyD88 和 NF-κB p65 的水平。用流式细胞术检测原代肝细胞中 NF-κB 的核转位水平。
BBR 可显著减轻肝组织脂肪变性和炎症细胞浸润；降低 NAFLD 活动评分和血清 ALT、AST、TC 和 LDL-C 水平；降低 TNF-α、IL-6 和 IL-1β水平，降低肝组织 TLR4、MyD88 和 NF-κB 表达。BBR 还可逆转原代肝细胞中 NF-κB 的核转位。
BBR 可缓解 NAFLD 及肝损伤的进展，可能通过 TLR4/MyD88/NF-κB 通路抑制 NF-κB 的核转位。
