黑木耳多糖提取物对肝纤维化大鼠肝功能及MPO, MDA, TGF-beta的影响

目的：探究黑木耳多糖提取物对肝纤维化大鼠血清髓过氧化物酶(MPO)、丙二醛(MDA)及转化生长因子beta(TGF-beta)的影响及肝功能的保护作用。方法：将健康的Wistar大鼠30 只随机分为3 组：对照组、模型组、黑木耳多糖提取物组，利用胆总管结扎术制备肝纤维化动物模型，术后分别用生理盐水0.1 mL/(kg·d)、黑木耳多糖提取物0.1 mg/(kg·d)灌胃1 次/d。21 d后腹主动脉采血，测肝功能指标，取肝组织测MDA、MPO、TGF-beta，Masson 染色。结果：肝纤维化动物模型成功制备。黑木耳多糖提取物组总胆红素(STB)、谷氨酸转移酶(ALT)、天门冬氨酸转移酶(AST)、MPO、MDA较模型组明显降低，TGF-茁含量降低。Masson 染色可见：模型组肝小叶结构破坏，较对照组汇管区可见大面积胶原纤维的形成；黑木耳多糖提取物组肝细胞轻度水肿、肝索排列欠整齐，肝汇管区及各部位胶原纤维形成量略少。结论：黑木耳多糖提取物可减轻胆总管结扎大鼠脂质过氧化损伤，MPO 含量使TGF-beta因子释放减少，从而减少胶原纤维形成，减轻或延缓大鼠肝纤维化。

Effects of Auricularia Auricula-judae Extract on Liver Function and MPO,MDA and TGF-beta of Rats with Hepatic Fibrosis

Objective:To explore the effects of Auricularia auricula-judae extracts on activities of MPO, MDA and TGF-beta in liverfibrosis rats and The protection of liver function.Methods:30 Wistar rats were randomly and equally divided into three groups: controlgroup (normal saline 0.1 mL/kg·d), model group (normal saline 0.1 mL/kg·d) and Auricularia auricula extract group (Auricularia auricular0.1 mg/kg·d), models of liver fibrosis were made to be bile duct ligation in rat collected blood from abdominal aorta to detected liverfunction after 21 days. Measure malondialdehyde (MDA), myeloperoxidase (MPO), transfer growth factor(TGF-beta) in liver tissue, Massonstaining observation.Results:Liver fibrosis animal model was duplicated in rats. Auricularia auricula extract group, total bilirubin,ALT, AST, MPO and MDA obviously lower (P<0.05), while TGF-beta decreased significantly compared with model group (P<0.05). Massonstaining: The structure of hepatic lobule was damaged in model group, collagen fibers formation in portal area compared with thecontrol group; Liver cells are slight edema in Auricularia auricula extract group, with hepatic plate arrangement disorder, less collagenfibers appear in the hepatic portal area.Conclusion:Auricularia auricula extract can reduce MPO and Lipid peroxidation damage makethe TGF-beta release is reduced, thus reducing the collagen formation, reduce or delay the liver fibrosis in rats.