甘草次酸对哮喘大鼠的抗氧化应激作用及NF-κB信号通路的调控

Effects of glycyrrhetinic acid on oxidative stress and NF-κB signal pathway in bronchial asthma rats

目的:探讨甘草次酸对哮喘大鼠肺组织NF-κB、IL-6、IL-5蛋白表达及抗氧化应激能力的影响。方法:采用卵清白蛋白致敏法制备大鼠支气管哮喘模型,并给予甘草次酸高、中、低(200、100、50 mg/kg)剂量进行干预;同时设正常对照和地塞米松对照;每组10只大鼠。干预7 d后处死大鼠,用生化法测大鼠血清超氧化物歧化酶(SOD)、丙二醛(MDA)、总抗氧化能力(T-AOC)及谷胱甘肽过氧化物酶(GSH-Px),用RT-PCR和Western-blot法测大鼠肺组织NF-κB、IL-6及IL-5 mRNA及蛋白表达水平。结果:与正常对照比较,模型组和GA各剂量组大鼠血清SOD、GSH-Px及T-AOC水平降低,MDA水平升高,肺组织中NF-κB、IL-6及IL-5 mRNA和蛋白表达水平升高(P<0.05)。与模型组比较,甘草次酸高、中剂量组大鼠血清SOD、GSH-Px水平升高,MDA水平降低(P<0.05),肺组织中NF-κB、IL-6及IL-5 mRNA和蛋白表达水平降低(P<0.05),其中甘草次酸高剂量组变化更显著。结论:甘草次酸对哮喘大鼠氧化应激有拮抗作用,其机制与调控NF-κB信号通路有关。

Aim： To investigate the effects of glycyrrhetinic acid（ GA） on the NF-κB signal pathway and anti-oxidative stress capability in experimental asthma rats. Methods： Ovalbumin allergization was used to establish bronchial asthma rat model,and the model rats were given GA（ 200,100,50 mg / kg） through intragastric administration once a day for 7 days,respectively,blank control,asthma model control and dexamethasone control were employed in the experiment,and 10 rats were in each group. The levels of SOD,MDA,GSH-Px and T-AOC in serum were determined by biochemical methods.The mRNA and protein expressions of NF-κB,IL-6 and IL-5 in lung tissue were determined by RT-PCR and Western blot,respectively. Results： Compared with the blank control group,the activity of SOD,GSH-Px and T-AOC in serum of asthma model control group and 3 GA groups decreased,the serum level of MDA was higher,and the mRNA and protein expressions of NF-κB,IL-6 and IL-5 in lung tissue were higher（ P〈0. 05）. Compared with the asthma model control group,the activity of SOD and GSH-Px in serum of 200 and 100 mg / kg GA group were higher,the serum level of MDA was lower,the mRNA and protein expressions of NF-κB,IL-6 and IL-5 in lung tissue were lower（ P〈0. 05）,and the changes of 200 mg / kg GA group were more obvious. Conclusion： GA has the capability to against oxidative stress in asthma rats,which may be related to the NF-κ B signal pathway.