天麻素通过HMGB1/TLR4/COX2通路调控创伤性脑损伤大鼠炎症反应

Gastrodin regulated inflammatory response in rats with traumatic brain injury through HMGB1/TLR4/COX2 signaling pathway

目的探究天麻素(GA)对大鼠创伤性脑损伤(TBI)引起的炎症反应的保护作用及其机制。方法30只健康雄性SD大鼠随机分成假手术组(Sham)、创伤性脑损伤组(TBI)和创伤性脑损伤+GA组(GA),采用控制性脑皮质撞击法(CCI)建立大鼠TBI模型。ELISA检测大鼠血清内炎症因子改变;HE染色观察组织病理学改变;Western blot技术检测炎症相关蛋白及HMGB1/TLR4/COX2信号通路相关蛋白表达。结果GA处理能够显著降低血清内炎症因子TNF-α、IL-1β和IL-6表达,减少脑组织炎症细胞浸润,降低脑组织内炎症相关蛋白NF-κB和S100β的表达,抑制HMGB1/TLR4/COX2信号通路激活(P<0.05)。结论GA对大鼠TBI所致炎症反应具有改善作用,其机制可能与抑制HMGB1/TLR4/COX2信号通路相关。

Objective To explore the effect and its potential mechanism of gastrodin(GA)on inflammatory response induced by traumatic brain injury(TBI)in rats.Methods Thirty healthy male SD rats were randomly divided into sham group(Sham),traumatic brain injury group(TBI)and traumatic brain injury with gastrodingroup(GA).Controlled cortical impact(CCI)was used to establish traumatic brain injury in mice.ELISA was used to detect the changes of inflammatory factors in serum of rats.HE staining was used to observe histopathological changes.Western blot technology was used to detect the expressions of HMGB1,TLR4 and COX2.Results GA treatment significantly reduced the levels of TNF-α,IL-1βand IL-6 in serum.The inflammatory cell infiltration in brain tissue was also reduced.HMGB1/TLR4/COX2 pathway was inhibited and expressions of NF-κB and S100βwere decreased(P<0.05).Conclusion GA treatment has a protective effect on TBI in mice,and its potential mechanism may be related to inhibition of the HMGB1/TLR4/COX2 signaling pathway.