雷公藤配伍金钱草对荷瘤状态下的相杀减毒机制研究  

Study on the mechanism of mutual detoxification of Tripterygium wilfordii Radix combined with Lysimachiae Herba in tumor-bearing state

作　　者：王君明[1,2] 蔡泓[1] 李金花[1] 陈荣幸 李金洋[1] 巫晓慧 张月月[1] 李军[3] 崔瑛[1,2] WANG Jun-ming;CAI Hong;LI Jin-hua;CHEN Rong-xing;LI Jin-yang;WU Xiao-hui;ZHANG Yue-yue;LI Jun;CUI Ying(College of Pharmacy,Henan University of Chinese Medicine,Zhengzhou 450046,China;Co-construction Collaborative Innovation Center for Chinese Medicine and Respiratory Diseases by Henan&Education Ministry of P.R.China,Henan University of Chinese Medicine,Zhengzhou,450046,China;Research and Experiment Center,Henan University of Chinese Medicine,Zhengzhou 450046,China)

机构地区：[1]河南中医药大学药学院,河南郑州450046 [2]河南中医药大学呼吸疾病中医药防治省部共建协同创新中心,河南郑州450046 [3]河南中医药大学科研实验中心,河南郑州450046

出　　处：《时珍国医国药》2020年第1期9-11,共3页Lishizhen Medicine and Materia Medica Research

基　　金：国家自然科学基金青年基金(81503269);河南中医药大学省属高校基本科研业务专项人才培养项目(2014KYYWF-QN01);河南中医学院博士科研基金(BSJJ2010-22)。

摘　　要：目的在荷瘤病理状态下观测雷公藤配伍金钱草的相杀减毒机制。方法通过对S180荷瘤小鼠血清肾功能指标以及肾组织氧化应激和炎症相关指标的比较分析,探讨雷公藤配伍金钱草的相杀减毒作用及其机制。结果雷公藤给药后诱导了S180荷瘤小鼠的血清肌酐(Cr)、尿素氮(BUN)、肾丙二醛(MDA)的水平均显著升高,以各配比(4/1~1/4)配伍金钱草给药后,均显著逆转了以上3个指标的异常(P<0.01);进一步机制分析显示,雷公藤诱导了荷瘤小鼠肾谷胱甘肽(GSH)、谷胱甘肽-S-转移酶(GST)、谷胱甘肽过氧化物酶(GPx)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、白介素(IL)-10的水平的显著降低(P<0.01)以及肿瘤坏死因子(TNF)-α水平的显著升高(P<0.01),而以各配比与金钱草配伍给药后,均显著逆转了以上7个指标的异常(P<0.01)。结论配伍金钱草对雷公藤所致的荷瘤小鼠的肾损伤具有减毒作用,其机制可能涉及增强荷瘤状态下肾的抗氧化防御并抑制炎症反应。Objective To observe the mutual detoxification mechanism of Tripterygium wilfordii Radix(LGT)via compatibility with Lysimachiae Herba(JQC)under the pathological state of tumor.Methods Through the comparative analysis of serum renal function indexes and renal tissue oxidative stress and inflammation related indexes in S180 tumor-bearing mice,the mechanism of their mutual detoxification was investigated.Results After LGT administration,the serum creatinine(Cr),urea nitrogen(BUN)and renal malondialdehyde(MDA)levels in S180 tumor-bearing mice were significantly increased,with ratios(4/1 to 1/4).After administration with JQC,the abnormalities of the above three indicators were significantly reversed(P<0.01).Further mechanism analysis showed that LGT induced significant reduction in renal glutathione(GSH),glutathione-S-transferase(GST),glutathione peroxidase(GPx),superoxide dismutase(SOD),catalase(CAT),and interleukin(IL)-10(P<0.01)and significant elevation in tumor necrosis factor(TNF)-α(P<0.01),and after the combination of each ratio and JQC,the abnormalities of the above seven indicators were significantly reversed(P<0.01)in S180 tumor-bearing mice.Conclusion-Compatibility with JQC has an attenuating effect on renal injury induced by LGT in tumor-bearing mice,and the mechanism may be related to enhancing the antioxidant defense and inhibiting the inflammatory response of the kidney under the tumor-bearing state.

关 键 词：荷瘤状态 减毒机制 肾损伤 抗氧化 炎症 

分 类 号：R285.5[医药卫生—中药学]