基于NF-κB信号通路探讨傣药龙血竭对急性乳腺炎的作用机制

Based on the NF-κB Signaling Pathway,The Mechanism of Dai Medicine Resina Draconis Exhaustion on Acute Mastitis Was Explored

目的:从核因子-κB(nuclear factor kappa-B,NF-κB)信号通路探讨傣药龙血竭对急性乳腺炎的治疗效果及其可能作用机制。方法:将18只大鼠随机分为空白组、模型组、龙血竭组,对后两组大鼠进行造模后,空白组、模型组乳房予生理盐水湿敷,龙血竭组予龙血竭药膏外敷。分别于第1天、第14天记录大鼠乳腺体积,取其血清检测C反应蛋白(CRP)、白介素-1β(IL-1β)、白介素-6(IL-6)、白介素-8(IL-8)、肿瘤坏死因子-α(TNF-α)水平,观察病理组织学变化。结果:与模型组比较,造模后24 h及治疗后第1天,龙血竭组肿块体积差异比较无统计学意义(P>0.05);治疗后第7天及第14天,龙血竭组大鼠肿块体积差异有显著统计学意义(P<0.001)。治疗14 d后,与模型组相比,龙血竭组IL-8水平差异无统计学意义(P>0.05);IL-1β、TNF-α水平差异具有统计学意义(P<0.05);CRP、IL-6水平差异具有显著统计学意义(P<0.01)。结论:龙血竭对急性乳腺炎具有治疗作用,其机制可能与其参与调控NF-κB信号通路有关。

Objective To investigate the therapeutic effect and possible mechanism of Dai medicine Resina Draconis exhaustion on acute mastitis from the nuclear factor-κB(NF-κB)signaling pathway.Methods Eighteen rats were randomly divided into blank group,model group and Resina Draconis group,and after modeling the rats in the latter two groups,the blank group and model group were given normal saline wet compress,and the Resina Draconis group was given Resina Draconis ointment for external application.The mammary gland volume of rats was recorded on the 1st and 14th days,and the serum levels of C-reactive protein(CRP),interleukin-1β(IL-1β),interleukin-6(IL-6),interleukin-8(IL-8)and tumor necrosis factor-α(TNF-α)were detected.Then the histopathological changes were observed.Results Compared with the model group,there was no significant difference in the volume of the mass in the Resina Draconis group at 24 h after modeling and the first day after treatment(P>0.05),and there was a significant difference in the volume of the mass in the Resina Draconis group on the 7th and 14th day after treatment(P<0.001).After 14 days of treatment,there was no significant difference in IL-8 levels in the Resina Draconis group(P>0.05),the difference in IL-1βand TNF-αlevels was statistically significant(P<0.05),and the difference in CRP and IL-6 levels was statistically significant(P<0.01).Conclusion Resina Draconis has a therapeutic effect on AM,and its mechanism may be related to its involvement in the regulation of NF-κB signaling pathway.