摘要
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.
Abstract
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 2 weeks 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-8 of 2%SA group was lower than 30%SA group and fusidic acid group(all P＜0.05).There was no significant difference in IL-8 between 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.
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