苦瓜对实验性大鼠肝纤维化的干预作用及可能机制

目的: 探讨苦瓜(BM)对四氯化碳(CCl₄)诱导大鼠肝纤维化的干预作用及相关机制。方法: 随机将32只雄性健康Wistar大鼠分为4组:对照组(C组);模型组(CCl₄,M组);BM低剂量组(BM 100g/kg饲料+CCl₄,BM-L组)、BM高剂量组(BM 200g/kg饲料+CCl₄,BM-H组)。饲养中除C组外的各组大鼠均皮下注射50%CCl₄-橄榄油溶液2 mL/kg,2次/周,共8周,诱导肝纤维化动物模型。8周后处死大鼠,留取大鼠肝脏和血清。计算肝体指数;测定血清丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性;测定肝匀浆总蛋白(TP)和白蛋白(Alb)含量、谷胱甘肽过氧化物酶(GSH-Px)活性、羟脯氨酸(HYP)含量和单胺氧化酶(MAO)活性;胶原纤维染色观察大鼠肝组织变性与胶原沉积病理改变。结果: 与M组比较,摄入BM后的各剂量组大鼠肝体指数显著降低(P<0.01);血清MDA含量及肝匀浆HYP含量和MAO活性均明显降低(P<0.01),而血清SOD活性、肝组织TP和Alb含量、GSH-Px活性明显增强(P<0.01)。与正常大鼠相比,模型大鼠肝脏有明显胶原沉积与肝纤维化,伴有不同程度的肝细胞炎性损伤坏死;BM组明显减轻模型大鼠肝组织损伤坏死与胶原沉积等病理变化,以高剂量组更明显。结论: BM具有抗CCl₄诱导大鼠肝纤维化作用,其机制可能与其抗脂质过氧化、降低肝HYP含量及MAO活性的作用有关。

Effect of bitter melon on liver fibrosis induced by carbon tetrachloride

AIM: To investigate the effects of bitter melon (BM) on liver fibrosis induced by CCl₄ in Wistar rats. METHODS: Healthy male Wistar rats were randomly divided into 4 groups (with 8 each): olive oil control group (group C), olive oil CCl₄ model group (group M), CCl₄+BM at low concentration (BM 100 g/kg, group BM-L), CCl₄+ BM at high concentration (BM 200 g/kg, group BM-H). All rats except those in group C were subcutaneously injected with CCl₄ twice a week for 8 weeks to induce liver fibrosis. After injection of CCl₄ for 8 weeks, all rats were sacrificed and the samples of blood and livers were collected. The weight ratio of liver to body was measured. The serum level of MDA and the activity of SOD were tested. The contents of total protein and albumin, the activity of GSH-Px, the content of hydroxyproline and the activity of monoamine oxidase in the liver homogenate were determined. Hepatic inflammation and collagen deposition were observed under microscope with Masson staining. RESULTS: In the rats treated with BM, the weight ratio of liver to body, the serum level of MDA, the content of hydroxyproline and the activity of monoamine oxidase in the liver homogenate were lower than those in group M (P<0.01). The serum activity of SOD, the contents of total protein and albumin, and the activity of GSH-Px in the liver homogenate were enhanced (P<0.01). The livers of the model rats had remarkable inflammatory necrosis, collagen accumulation and fibrosis. The rats in BM-treated group showed slighter hepatic injury and collagen deposition, and the liver functions were much better than those in the model group. High dose of BM showed more obvious liver-protective effects. CONCLUSION: BM attenuates liver fibrosis by its antioxidant effect and the mechanisms of reducing hydroxyproline content and monoamine oxidase activity.