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目的观察白英乙醇提取物(EEST)对四氯化碳(CCl4)诱导大鼠急性肝坏死的影响。方法将Wistar大鼠分为五组,每组10只。对照组(A组)、CCl4组(B组)、150 mg/kg EEST+CCl4组(C组)、300 mg/kg EEST+CCl4组(D组)和50 mg/kg Silibinin+CCl4组(E组)灌胃7 d,1次/d,0.5 ml/次,最后1 d,A组腹腔注射生理盐水,余各组腹腔注射CCl4 1 ml/kg。16 h后检测血清中丙氨酸氨基转移酶(ALT)、天冬氨酸氨基酸转移酶(AST)、碱性磷酸酶(ALP);肝组织苏木素-伊红(HE)染色观察病变程度;黄嘌呤氧化酶法和硫代巴比妥酸法分别检测肝匀浆中超氧化物岐化酶(SOD)、过氧化氢酶(CAT)和丙二醛(MDA)。结果与A组比较,B组血清中ALT、AST、ALP的含量显著增加,差异有统计学意义(P<0.05),HE染色肝组织变性坏死累及全小叶。与B组比较,C、D、E组血清中ALT、AST、ALP的含量显著下降,差异有统计学意义(P<0.05),HE染色病变程度较轻;胞浆中SOD和CAT活性提高、MDA水平降低,差异有统计学意义(P<0.05)。结论 EEST能显著减轻CCl4诱导的肝损伤,可能与EEST抗脂质过氧化作用有关。
Objective To observe the effect of EEST on acute liver necrosis induced by carbon tetrachloride (CCl4) in rats. Methods Wistar rats were divided into five groups of 10 rats. The rats in control group (group A), CCl4 group (group B), 150 mg / kg EEST + CCl4 group (C group), 300 mg / kg EEST group and CCl4 group (D group) and 50 mg / kg Silibinin + Group) for 7 d, once / d and 0.5 ml / time for the last 1 d. Rats in group A were injected intraperitoneally with saline, and the rest were intraperitoneally injected with 1 ml / kg of CCl4. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were detected after 16 h. Liver lesions were observed by hematoxylin-eosin staining. Purine oxidase method and thiobarbituric acid method were used to detect superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA) in liver homogenate respectively. Results Compared with group A, the levels of ALT, AST and ALP in group B were significantly increased (P <0.05). The degeneration and necrosis of hepatic tissue in HE group involved the whole leaflets. Compared with group B, the contents of ALT, AST and ALP in group C, D and E were significantly decreased (P <0.05), and the degree of lesion in HE staining was lighter; the activity of SOD and CAT in cytoplasm increased, MDA level decreased, the difference was statistically significant (P <0.05). Conclusion EEST can significantly reduce CCl4-induced liver injury, which may be related to the anti-lipid peroxidation of EEST.