中文摘要：

目的：探讨柴胡皂苷d（SSd）对二甲基亚硝胺（DMN）所致肝纤维化大鼠肝组织中超氧化物歧化酶（SOD）、丙二醛（MDA）的含量与血清中微量元素锌、钙的影响。方法：以DMN腹腔内注射每周2次,持续6周,建立肝纤维化模型。SSd治疗组注射DMN2周后同时每天SSdip治疗4周。取肝组织进行病理检查,免疫组化法观察TGF-β1、α-SMA在肝组织中的表达;分光光度比色法检测肝组织匀浆中MDA、SOD的水平;采用原子吸收分光光度计测定血清中锌、钙微量元素的含量。结果：与模型组比较,SSd治疗组能明显减轻大鼠肝纤维化的程度,显著降低肝组织中TGF-β1、α-SMA蛋白的表达,降低肝组织中MDA含量,有升高SOD活性的趋势;并可使血清中微量元素锌水平升高、钙水平降低。结论：SSd能减轻DMN诱导的大鼠肝纤维化程度,其可能的机制与干预了肝内脂质过氧化反应和调节血清中微量元素锌、钙的水平有关。

英文摘要：

To investigate the anti-fibrotic effects of saikosaponin-d （SSd） with the relationship between MDA,SOD in liver tissue and zine,calcium content in the serum. Methods：Rats were randomized into normal group, model group and SSd-treated group. Model group and SSd-treated group were intraperitoneally injected with 0.5mg/kg DMN per rat, two times in one week for 6 weeks. After 2 weeks, the SSd-treated group were given intraperitoneal injection of 1.8mg/kg SSd per rat, once daily for 4 weeks. While the normal group were intraperitoneally injected with saline, once daily for 6 weeks. Liver samples were taken for the observation of pathology, the levels of MDA, SOD were measured by chromatometry, and the contents of Zn and Ca were determined by atomic absorption spectrometry. The expressions of TGF-β 1 and α-SMA were detected by immunohistochemistry method. Results： Compared with the model group, SSd could significandy reduce the expression of TGF-β1 and α-SMA, improve the degree of fibrosis, decrease the level of MDA, while increase the activity of SOD gradually and adjust the contents of Zn and Ca. Conclusion ： SSd can evidendy improve the progression of hepatic fibrosis. The mechanism of such effects is related to inhibit expression of TGF-β 1 and α-SMA , affect lipid preoxidation and adjust the contents of Zn and Ca.