超分子水杨酸对兔耳痤疮模型p38MAPK/NF-κB信号通路的影响

Effect of Supramolecular Salicylic Acid on p38MAPK/NF-κB Signaling Pathway in Rabbit Ear Acne Models

目的:探究超分子水杨酸对兔耳痤疮模型p38MAPK/NF-κB信号通路的影响机制。方法:将30只实验兔随机分成正常对照组、2%超分子水杨酸(Salicylic acid,SA)组、30%SA组、夫西地酸组、模型对照组,每组6只,并予以相应外用药物干预,连续4周,并分别于用药2周后、用药4周后检测p38MAPK、NF-κB、IL-1β、IL-8蛋白的表达。结果:结果显示,随着用药时间的延长,各组的p38MAPK、NF-κB、IL-1β、IL-8均呈下降趋势。用药前,各组间p38MAPK、NF-κB、IL-1β、IL-8蛋白表达均差异无统计学意义(P>0.05)。用药2周后,2%SA组、30%SA组、夫西地酸组p38MAPK、NF-κB、IL-1β、IL-8低于模型对照组(P<0.001);三个用药组之间p38MAPK、NF-κB、IL-1β两两比较差异无统计学意义(P>0.05);2%SA组IL-8低于30%SA组、夫西地酸组(均P<0.05);30%SA组与夫西地酸组IL-8差异无统计学意义(P>0.05)。用药4周后,三个用药组p38MAPK、NF-κB、IL-1β、IL-8低于模型对照组(P<0.05);2%SA组、30%SA组p38MAPK、NF-κB、IL-8低于夫西地酸组(P<0.05),2%SA组IL-8低于30%SA组(P<0.05);2%SA组与30%SA组p38MAPK差异无统计学意义(P>0.05);2%SA组、30%SA组与夫西地酸组IL-1β均差异无统计学意义(均P>0.05);2%SA组IL-1β低于30%SA组,差异具有统计学意义(P<0.05)。结论:超分子水杨酸可通过抑制p38MAPK/NF-κB信号通路来发挥抗炎作用,且随着用药时间的延长疗效也在逐渐增加,并优于夫西地酸。

Objective To explore the effect of supramolecular salicylic acid on p38MAPK/NF-κB signaling pathway in rabbit ear acne model. Methods Divided thirty experimental rabbits into normal control group, 2%SA group, 30%SA group,fusidic acid group and model control group(There were 6 rabbits in each group) randomly. Gave corresponding external drug intervention for 4 weeks. Detected the expressions of p38MAPK, NF-κB, IL-1β and IL-8 after 2 weeks and 4 weeks. Results Result display, P38MAPK, NF-κB, IL-1β, and IL-8 of each group showed a downward trend after treatment. Before treatment,there were no significant differences in expression of p38MAPK, NF-κB, IL-1β and IL-8 among groups(P>0.05). After 2weeks of treatment, p38MAPK, NF-κB, IL-1β, and IL-8 of 2% SA group, 30% SA group and fusidic acid group were lower than model control group(P<0.001). There were no significant differences in p38MAPK, NF-κB, and IL-1β(P>0.05). IL-8of 2% SA group was lower than 30% SA group and fusidic acid group(all P<0.05). There was no significant difference in IL-8between 30% SA group and fusidic acid group(P>0.05). After 4 weeks of treatment, p38MAPK, NF-κB, IL-1β, and IL-8 of three treatment groups were lower than model control group(P<0.05). p38MAPK, NF-κB, IL-8 of 2% SA group and 30% SA group was lower than fusidic acid group(P<0.05), IL-8 of 2%SA group was lower than 30%SA group(P<0.05). There was no significant difference in p38MAPK between 2%SA group and 30%SA group(P>0.05). 2% SA group, 30% SA group and fusidic acid group had no significant difference in IL-1β(all P>0.05). 2%SA group IL-1β was lower than 30%SA group, the difference was Statistical significance(P<0.05). Conclusion Supramolecular salicylic acid can exert an anti-inflammatory effect by inhibiting the p38MAPK/NF-κB signaling pathway, and the curative effect gradually increases with the prolongation of medication time, and is superior to fusidic acid.