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目的考察川楝子致大鼠肝脏损害的毒性机制。方法将大鼠随机分组,薄荷油组口服薄荷油致肝毒性剂量2.4ml/kg,四氯化碳组口服四氯化碳2.5ml/kg,正常组给予同容积溶媒。给药36或48h后,取血,用ELISA法检测血清TNF-α、IL-6含量;取肝组织,用免疫组化法检测肝组织NF-κB、ICAM-1蛋白表达。结果(1)与正常组相比,薄荷油组与四氯化碳组大鼠血清TNF-α、IL-6含量显著升高(P<0.01)。(2)与正常组比较,薄荷油组与四氯化碳组大鼠肝组织NF-κB、ICAM-1蛋白表达显著增强(P<0.01)。结论大鼠一次性口服薄荷油2.4ml/kg,可引起血清TNF-α、IL-6升高,肝组织NF-κB、ICAM-1蛋白表达增强。炎症反应可能是薄荷油致肝毒性的机制之一。
Objective To investigate the toxic mechanism of liver damage caused by Chuanxiongzi in rats. Methods The rats were randomly divided into two groups. The dose of hepatotoxicity was 2.4ml/kg in peppermint oil group and 2.5ml/kg in carbon tetrachloride group. The normal group was given the same volume of vehicle. After 36 or 48 hours of administration, blood was taken and serum TNF-α and IL-6 levels were measured by ELISA. Liver tissues were taken and the expression of NF-κB and ICAM-1 proteins was detected by immunohistochemistry. Results (1) Compared with the normal group, the levels of serum TNF-α and IL-6 in peppermint oil group and carbon tetrachloride group were significantly increased (P<0.01). (2) Compared with the normal group, the expression of NF-κB and ICAM-1 in liver tissue of peppermint oil group and carbon tetrachloride group were significantly increased (P<0.01). CONCLUSION: One-time oral administration of peppermint oil 2.4 ml/kg in rats can increase serum TNF-α and IL-6 levels, and increase the expression of NF-κB and ICAM-1 protein in liver tissue. The inflammatory response may be one of the mechanisms of hepatotoxicity induced by peppermint oil.