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目的:探讨海兔素对刀豆蛋白A诱导的化学性肝损伤保护作用。方法:雄性Wistar大鼠随机分为4组。模型组与海兔素组给予15 mg/kg刀豆蛋白A尾静脉注射每周一次,制作化学性肝损伤模型,模型制作成功后,正常对照组、模型组每日给予大豆油灌胃,海兔素低、高剂量组给予100、150 mg/kg·d海兔素+大豆油灌胃。实验持续8周后,禁食12 h,处死大鼠。HE染色观察肝组织形态学改变;Masson Trichrome及天狼星红染色观察肝组织纤维化状况;全自动生化分析仪检测血清ALT、AST及LDH水平;ELISA实验测定血清TNF-α和TGF-β1水平。结果:与正常对照组相比,模型组大鼠肝小叶结构模糊紊乱,纤维组织增生明显,可见灶状坏死及炎性细胞浸润,胶原纤维明显增多,胶原指数明显升高。血清中ALT、AST、LDH及TNF-α和TGF-β1水平显著升高(P<0.05)。海兔素干预后,肝小叶病变程度较模型组明显减轻,染色胶原显著减少,纤维增生明显改善,血清中ALT、AST、LDH及TNF-α和TGF-β1水平较模型组显著降低(P<0.05),海兔素高剂量组与低剂量组相比,肝脏病变改善程度更为明显(P<0.05)。结论:海兔素对刀豆蛋白A诱导的化学性肝损伤具有一定保护作用,其机制可能与下调TNF-α、TGF-β1水平有关。
Objective: To investigate the protective effect of sea-rabbit on chemical liver injury induced by concanavalin A. Methods: Male Wistar rats were randomly divided into 4 groups. The model group and the sea-rabbit group were given 15 mg / kg concanavalin A intravenous injection once a week to make a chemical liver injury model. After successful model making, the normal control group and the model group were given daily soybean oil orally, sea Rabbit low, high dose group given 100,150 mg / kg · d sea Rabbit + soybean oil gavage. After 8 weeks, the rats were fasted for 12 hours and sacrificed. Liver histomorphology was observed by HE staining. Liver fibrosis was observed by Masson Trichrome and Sirius red staining. Serum levels of ALT, AST and LDH were detected by automatic biochemical analyzer. Serum levels of TNF-α and TGF-β1 were measured by ELISA. Results: Compared with the normal control group, the hepatic lobule structure of the model group was obscured and the fibrous tissue hyperplasia was obvious. The focal necrosis and inflammatory cell infiltration were seen. The collagen fibers increased obviously and the collagen index increased obviously. Serum ALT, AST, LDH and TNF-α and TGF-β1 levels were significantly increased (P <0.05). Compared with the untreated group, the severity of hepatic lobule lesion was significantly reduced after treatment with dexamethasone, the number of stained collagen was significantly decreased, the proliferation of fibrosis significantly improved, and the levels of ALT, AST, LDH, TNF-α and TGF-β1 in serum were significantly lower than those in model group (P < 0.05). Compared with the low dose group, the hippocampus high dose group showed a more significant improvement of liver lesion (P <0.05). CONCLUSION: Hyponatremia has a protective effect on hepatotoxicity induced by concanavalin A, and its mechanism may be related to down-regulating the levels of TNF-α and TGF-β1.