参芎葡萄糖注射液及其丹参组分对小鼠核受体表达的调控作用

Effects of Shenxiong Glucose Injection and the component of Salvia miltiorrhiza in regulation of nuclear receptor expression in mice liver

目的考察参芎葡萄糖注射液(SGI)及其丹参组分(SM)对小鼠肝细胞中芳香烃受体(Ah R)、肝细胞核因子4α(HNF-4α)、孕烷X受体(PXR)和过氧化物酶体增殖物激活受体α(PPARα)m RNA表达的影响。方法采用随机数表法将40只雄性小鼠分为8组,每组5只,分别为空白组、阳性组(苯巴比妥)、SGI低剂量组(以丹参素计2.6 mg·kg^(-1)·d^(-1))、SGI中剂量组(以丹参素计3.9 mg·kg^(-1)·d^(-1))、SGI高剂量组(以丹参素计5.2 mg·kg^(-1)·d^(-1))、SM低剂量组(以丹参素计2.6 mg·kg^(-1)·d^(-1))、SM中剂量组(以丹参素计3.9 mg·kg^(-1)·d^(-1))、SM高剂量组(以丹参素计5.2 mg·kg^(-1)·d^(-1)),连续给药7 d。提取各组小鼠肝脏组织中的RNA,检测相关核受体m RNA的变化。结果与空白组相比,SGI高剂量组可以上调Ah R m RNA的水平(P<0.05),上调倍数为1.7倍,但是SGI对PPARα、PXR、HNF-4α的m RNA水平没有显著性影响(P>0.05);SM对Ah R、PPARα、PXR和HNF-4α的m RNA表达均无显著性影响(P>0.05)。结论高剂量的参芎葡萄糖注射液能够影响Ah R m RNA的表达,但这种影响并不是由其丹参组分导致的。

Objective To investigate the effects of Shenxiong Glucose Injection（SGI） and Salvia miltiorrhiza（SM） on the expressions of aryl hydrocarbon receptor（Ah R）, hepatic nuclear factor 4 alpha（HNF-4α）, pregnane X receptor（PXR） and peroxisome proliferator activatedreceptor-α（PPAR α） m RNA in mice livers. Methods Mice were divided into blank group, positive group（phenobarbital）, SGI and SM different dosage groups of low-dose SGI group(2.6 mg·kg-1·d-1SM), medium-dose SGI group(3.9 mg·kg-1·d-1SM), high-dose SGI group(5.2 mg·kg-1·d-1SM)and low-dose SM group(2.6 mg·kg-1·d-1SM), medium-dose SM group(3.9 mgv·kg-1·d-1SM), high-dose SM group(5.2 mg·kg-1·d-1SM), according to the random number table. Then the mice were killed after being administered medicines once daily for consecutive 7 days. Livers were prepared to determine the expression levels of Ah R, HNF-4α, PXR and PPARα m RNA by quantitative real-time PCR in mice. Results Compared with the blank group, Ah R m RNA were increased by 1.7 times in the high-dose SGI group（P<0.05）. SGI was found to have no impact on the expressions of HNF-4α, PXR and PPARα m RNA（P>0.05）, and SM was found to have no impact on the expressions of Ah R, HNF-4α,PXR and PPAR α m RNA（P>0.05）. Conclusion SGI of high dose could upregulate the expression of Ah R m RNA in mice livers, which is not contributed by SM.