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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。
Objective: To investigate the effects of saikosaponin d (SSd) on the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in liver tissue of rats with hepatic fibrosis induced by dimethylnitrosamine (DMN) Element of zinc, the impact of calcium. Methods: The model of hepatic fibrosis was established by intraperitoneal injection of DMN twice a week for 6 weeks. The SSd treatment group was treated with SSdip for 2 weeks after DMZ injection for 4 weeks. The liver tissue was taken for pathological examination. The expression of TGF-β1 and α-SMA in liver tissue was observed by immunohistochemistry. The levels of MDA and SOD in liver homogenate were detected by spectrophotometry. The atomic absorption spectrophotometer Serum zinc, calcium trace elements content. Results: Compared with the model group, SSd treatment group could significantly reduce the degree of hepatic fibrosis in rats, significantly reduce the expression of TGF-β1, α-SMA protein in liver tissue, reduce the content of MDA in liver tissue, increase the activity of SOD Trend; and serum zinc can increase trace elements, calcium levels decreased. Conclusion: SSd can reduce the degree of hepatic fibrosis induced by DMN in rats. The possible mechanism is related to the intrahepatic lipid peroxidation and the regulation of serum zinc and calcium levels.