白刺果提取物花色苷通过抑制肝脏纤维化及炎症减轻非酒精性脂肪性肝病

目的:探讨白刺果提取物花色苷对高脂饮食导致的小鼠非酒精性脂肪肝的治疗作用和潜在机制。方法:高脂饮食建立小鼠非酒精性脂肪肝模型,用花色苷进行干预后,测量小鼠肝脏重量,检测小鼠血清中丙氨酸氨基转移酶(ALT)和天门冬氨酸氨基转移酶(AST)、甘油三酯(TG)、总胆固醇(TC)和低密度脂蛋白胆固醇(LDL-C)含量;肝脏组织经过HE染色、油红O染色及Masson染色,观察小鼠组织形态、脂滴沉积和胶原纤维增生的情况;Western blot检测肝脏组织中炎症因子肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)、IL-6及IL-10的水平;免疫组化检测肝脏组织中巨噬细胞、白细胞和单核细胞的浸润情况及肝脏组织趋化因子CCL7和单核细胞趋化蛋白1(MCP-1)的表达。结果:白刺果提取物花色苷能显著抑制由高脂饮食引起的小鼠肝重、ALT、AST、TG、TC及LDL-C的增高;肝脏切片染色显示花色苷能缓解由高脂饮食引起的肝脏纤维化及炎性细胞的浸润;花色苷能降低肝脏中炎症因子TNF-α、IL-1β、IL-6和IL-10及炎性趋化因子CCL7和MCP-1的水平。结论:白刺果提取物花色苷显著缓解由高脂饮食引起的非酒精性脂肪性肝病,其机制主要是通过抑制肝脏中的炎性因子和炎性细胞的浸润并降低炎性趋化因子来实现的。

Anthocyanins attenuates hepatic fibrosis and inflammation in non-alcoho-lic fatty liver disease mice

AIM: To explore the therapeutic effect of anthocyanins from Fructus Acanthophorae on high-fat diet-induced non-alcoholic fatty liver disease(NAFLD) in mice and the potential mechanism. METHODS: NAFLD mouse model was established by high-fat diet, and interferred with anthocyanins. The liver weight, and serum aspartate aminotransferase(AST), alanine aminotransferase(ALT), triglyceride(TG), total cholesterol(TC) and low-density li-poprotein cholesterol(LDL-C) were measured. The liver tissues were staining with HE, Oil Red O and Masson’s trichrome. The protein levels of inflammatory factors tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), IL-6 and IL-10 in the liver tissues were determined by Western blot. The liver macrophage, white blood cell and mononuclear cell infiltration was detected by immunohistochemical method. The chemokines CCL7 and MCP-1 were also measured by immunohistochemical method. RESULTS: Anthocyanins significantly inhibited the increases in the liver weight, ALT, AST, TG, TC and LDL-C induced by high-fat diet. Anthocyanins attenuated the liver fibrosis and inflammatory cell infiltration caused by high-fat diet, and reduced the levels of inflammatory factors TNF-α, IL-1β, IL-6, IL-10 and inflammatory chemokines CCL7 and MCP-1 in the liver tissues. CONCLUSION: Anthocyanins significantly alleviate non-alcoholic fatty liver disease caused by high-fat diet though reducing inflammatory factors, inflammatory cell infiltration and inflammatory chemokines.