摘要
目的:研究龙胆苦苷(GPS)对胆汁淤积大鼠的干预和调节作用,为GPS的临床应用提供一定的实验依据。方法:将60只SD大鼠随机分为6组:正常对照组、模型组、阳性对照组(熊去氧胆酸,100 mg·kg^-1)、GPS高、中、低剂量组(200,100,50mg·kg^-1),每组10只。除正常对照组和模型组大鼠每日灌胃等体积的羧甲基纤维素钠(CMC-Na)溶液外,其余各组大鼠按相应剂量连续灌胃7 d,3次/d。在第5天除正常对照组外的其余各组大鼠一次性灌胃α-荼基异硫氰酸盐(ANTI)100 mg·kg^-1建立胆汁淤积大鼠模型。造模后48 h检测大鼠胆汁流量变化;检测血清中丙氨酸氨基转移酶(ALT)、门冬氨酸氨基转移酶(AST)、总胆红素(TBIL)、直接胆红素(DBIL)、总胆汁酸(TBA)含量;检测血清中炎症因子肿瘤坏死因子(TNF-α)、白细胞介素1β(IL-1β)的表达;观察肝脏组织病理变化;检测肝脏组织中脂质过氧化物丙二醛(MDA)及氧化酶超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的含量。结果:与模型组比较,GPS能改善肝脏组织病理损伤,促进胆汁排泄,降低模型大鼠血清中ALT、AST、TBIL、DBIL、TBA水平、MDA的含量及炎症因子TNF-α、IL-1β的表达,升高大鼠肝脏组织匀浆中SOD和GSH-Px的活性(P<0.05或P<0.01),各指标变化呈剂量依赖性。结论:GPS能够通过改善肝脏病理损伤及胆汁排泄量和降低血清酶的活性来治疗肝损伤,其保护机制与缓解体内氧化应激、降低炎症表达有关。
Objective:To study the effects of gentiopicroside(GPS)on ANIT-induced cholestasis in rats to provide experimental basis for the clinical application of GPS.Methods:Totally 60 SD rats were randomly divided into 6 groups:normal control group,model group,positive control group(ursodeoxycholic acid,100 mg·kg^-1),and GPS high,medium and low dose groups(200,100,50 mg·kg^-1)with 10 ones in each group.Except the rats in the normal control group and the model group were treated with the equal volume of carboxymethylcellulose sodium(CMC-Na)solution every day,rats in the other groups were given the corresponding drug for 7 days,three times a day.On the 5 th day,the rats in each group except the normal control group were given 100 mg·kg^-1α-naphthylisothiocyanate once to establish the model of cholestasis.The changes of bile flow in rats were detected 48 hours after model establishment;the contents of alanine aminotransferase(ALT),aspartate aminotransferase(AST),total bilirubin(TBIL),direct bilirubin(DBIL)and total bile acid(TBA)in serum were detected;the expressions of inflammatory factors,tumor necrosis factor(TNF-alpha)and interleukin-1β(IL-1β)in serum were detected.The pathological changes of liver tissues were observed and the contents of lipid peroxide malondialdehyde(MDA),oxidase superoxide dismutase(SOD)and glutathione peroxidase(GSH-Px)in liver tissues were detected.Results:Compared with the model group,GPS could improve liver tissue pathological damage,promote bile excretion and reduce the serum levels of ALT,AST,TBIL,DBIL and TBA,the content of MDA and the expressions of inflammatory factors TNF-αand IL-1βin serum of model rats,increase the activities of SOD and GSH-Px in rat’s liver tissue homogenate(P<0.05 or P<0.01),and the changes of each index were dose-dependent.Conclusion:GPS can treat liver injury by improving liver pathological damage,improving bile excretion and reducing serum enzyme activity.Its protective mechanism is related to alleviating oxidative stress and reducing inflammation expressio
作者
丁洁
Ding Jie(Department of Pharmacy,Mianyang Central Hospital,Sichuan Mianyang 621000,China)
出处
《中国药师》
CAS
2020年第11期2133-2137,共5页
China Pharmacist
