摘要
目的:观察星状神经节阻滞(SGB)对急性腹膜炎(AP)大鼠血清炎症因子的影响以及toll样受体4(TLR4)蛋白、半胱氨酸天冬氨酸蛋白酶3(caspase-3)、NF-κB(p65)蛋白表达情况,旨在深入探讨SGB对大鼠急性腹膜炎炎症反应的作用机制。方法:40只SPF级雄性大鼠依据随机化原则分为4组:对照组(Control)、急性腹膜炎组(AP)、急性腹膜炎+右侧颈交感干离断组(AP+SGB)、急性腹膜炎+右侧颈交感干离断+TLR4抑制剂瑞沙托维组(AP+SGB+TAK-242),每组10只。向AP组、AP+SGB组和AP+SGB+TAK-242组大鼠的腹腔内分别注射2%冰醋酸溶液1 ml/100 g,建立急性腹膜炎模型。成功造模后,分别于1、6、12和24 h取大鼠尾静脉血。ELISA法检测血清中白细胞介素-10(IL-10)、肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)和高迁移率族蛋白B1(HMGB1)的浓度。实验24 h后取腹膜组织,Western Blot法检测TLR4蛋白、caspase-3和NF-κB(p65)蛋白水平,RT-qPCR法检测TLR4 mRNA和NF-κB(p65) mRNA的表达情况,HE染色和光学显微镜观察病理变化。结果:与Control组相比,各时间点AP组、AP+SGB组和AP+SGB+TAK-242组IL-10、TNF-α、IL-1β、HMGB1水平显著升高(P<0.05);相同时间点内,AP+SGB组较AP组TNF-α、IL-1β、HMGB1水平显著降低,IL-10水平显著升高(P<0.05);与AP+SGB组相比,AP+SGB+TAK-242组TNF-α、IL-1β、HMGB1水平进一步降低,IL-10水平进一步升高(P<0.05)。AP+SGB组与AP+SGB+TLR组TLR4蛋白、caspase-3、NF-κB(p65)蛋白表达显著减少(P<0.05),且其TLR4 mRNA和NF-κB(p65) mRNA表达水平均明显下降(P<0.05)。结论:SGB可以通过抑制TLR4、NF-κB(p65)介导的TLR4/NF-κB信号通路来缓解大鼠急性腹膜炎的炎症反应。
Objective:To investigate the effects of stellate ganglion block(SGB)on serum inflammatory cytokines and the expression of toll-like receptor 4(TLR4),cysteine aspartate protease 3(caspase-3),and NF-κB(p65)proteins in rats with acute peritonitis(AP),with the goal of elucidating the mechanisms through which SGB modulates inflammatory responses.Methods:40 SPF grade male rats were randomly assigned to 4 groups:control group(Control),acute peritonitis group(AP),acute peritonitis+right stellate ganglion block group(AP+SGB),and acute peritonitis+right stellate ganglion block+TLR4 inhibitor resatorvid group(AP+SGB+TAK-242),with 10 rats in each group.Acute peritonitis was induced in the AP,AP+SGB,and AP+SGB+TAK-242 groups via intraperitoneal injection of 1 ml/100 g of 2%acetic acid solution.After establishing the model,blood samples were collected from the tail vein at 1 h,6 h,12 h,and 24 h respectively.Serum levels of interleukin-10(IL-10),tumor necrosis factor-alpha(TNF-α),interleukin-1β(IL-1β),and high mobility group protein B1(HMGB1)were measured using ELISA.After 24 hours,the peritoneal tissues were collected for analysis.Protein levels of TLR4,caspase-3,and NF-κB(p65)were quantified via Western Blot,while simultaneously,their mRNA expression levels were assessed using RT-qPCR.Histopathological alterations were evaluated by hematoxylin and eosin(HE)staining and then observed under optical microscopy.Results:At all time points,the AP,AP+SGB,and AP+SGB+TAK-242 groups showed significantly higher levels of IL-10,TNF-α,IL-1β,and HMGB1 compared to the S group(P<0.05).The AP+SGB group exhibited significantly lower TNF-α,IL-1β,and HMGB1 levels and higher IL-10 levels than the AP group at corresponding time points(P<0.05).The AP+SGB+TLR4 group demonstrated further reductions in TNF-α,IL-1β,and HMGB1 levels and additional increases in IL-10 levels relative to the AP+SGB group(P<0.05).Both the AP+SGB and AP+SGB+TAK-242 groups showed significant decreases in TLR4,caspase-3,and NF-κB(p65)protein expression(P<0.05).Similarly,TLR4 and NF-κB(p65)mRNA expression levels were markedly downregulated in these groups(P<0.05).Conclusion:SGB can mitigate the inflammatory response in acute peritonitis rats by inhibiting the TLR4/NF-κB signaling pathway through the downregulation of TLR4 and NF-κB(p65).
作者
杨鹏
曹宇
金璐薇
李林
邹学军
YANG Peng;CAO Yu;JIN Luwei;LI Lin;ZOU Xuejun(Department of Anesthesiology,Affiliated Renhe Hospital of China Three Gorges University,Yichang 443001,China)
出处
《神经解剖学杂志》
CSCD
北大核心
2024年第6期754-760,共7页
Chinese Journal of Neuroanatomy
基金
湖北省自然科学基金(2023AFC021)。
