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小檗碱调控TLR4/p38MAPK通路促进脑缺血再灌注大鼠神经功能恢复 被引量:3

Berberine Promotes Neural Function Recovery in Cerebral Ischemia-reperfusion Rats by Regulating the TLR4/p38 MAPK Pathway
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摘要 目的 观察小檗碱对脑缺血再灌注损伤大鼠的神经保护作用并探索其作用机制。方法 SD大鼠45只,随机分为假手术组(sham)、模型组(MCAO/R)、小檗碱治疗组(Ber)。通过线栓法建立脑缺血再灌注模型。Ber组给药剂量为140 mg/kg。给药28 d后应用Zea-longa评分和旋转棒实验评估大鼠神经功能。给药24 h后通过TTC染色观察并统计梗死面积。给药24 h后取材大鼠脑组织,应用免疫荧光染色观察白介素1β(interleukin 1β,IL-1β)的表达,应用免疫酶联吸附实验(enzyme linked immunosorbent assa, ELISA)检测IL-1β、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、和白细胞介素-6(interleukin 6,IL-6)、白细胞介素-10(interleukin 10,IL-10)的含量,通过Western Blot方法检测各组脑组织中TLR4、P-p38MAPK、p38MAPK蛋白含量。结果 Zea-longa评分和旋转棒实验结果证明小檗碱显著改善脑缺血再灌注损伤大鼠的运动能力。TTC染色结果表明小檗碱减少梗死面积。免疫荧光染色和ELISA实验结果证实小檗碱能够减少缺血损伤脑组织中促炎因子IL-1β、TNF-α、IL-6的含量,增加抗炎因子IL-10的含量。Western Blot结果提示小檗碱影响TLR4/p38MAPK通路蛋白的表达。结论 小檗碱通过TLR4/p38MAPK信号通路抑制MCAO/R大鼠脑组织中炎症因子的分泌,促进缺血再灌注大鼠神经功能恢复。 Objective To observe the neuroprotective effect of berberine on rats with cerebral ischemia-reperfusion injury and explore its mechanism of action.Methods 45 SD rats were randomly divided into three groups:sham surgery group(sham),model group(MCAO/R),and berberine treatment group(Ber).A cerebral ischemia-reperfusion model was established using the suture method.The dosage of Ber group was 140mg/kg.After 28 days of administration,Zea-longa score and rotating rod experiment were used to evaluate the neural function of rats.After 24 hours of administration,the infarct area was observed and calculated through TTC staining.After 24 hours of administration,brain tissue samples were taken from rats.Immunofluorescence staining was used to observe the expression of interleukin 1β(IL-1β),enzyme linked immunosorbent assay(ELISA)was used to detect the content of IL-1β,tumor necrosis factor-α(TNF-α),interleukin 6(IL-6)and interleukin-10(IL-10),and Western Blot was used to detect the protein contents of TLR4,P-p38MAPK and p38MAPK in brain tissues of each group.Results The results of the Zea-longa score and the rotating rod experiment showed that berberine significantly improved the motor ability of rats with cerebral ischemia-reperfusion injury.The TTC staining results showed that berberine reduced the infarct area.The results of immunofluorescence staining and ELISA experiments confirm that berberine can reduce the pro-inflammatory factor IL-1β、TNF-α、IL-6,and increases the content of anti-inflammatory factor IL-10.The Western Blot results suggest that berberine affects the expression of TLR4/p38MAPK pathway proteins.Conclusion Berberine inhibits the secretion of inflammatory factors in the brain tissue of MCAO/R rats through the TLR4/p38MAPK signaling pathway,promoting the recovery of neurological function in ischemia-reperfusion rats.
作者 冯慧聪 高娜娜 宋小峰 Feng Huicong;Gao Nana;Song Xiaofeng(School of Basic Medicine,Jinzhou Medical University,Jinzhou 121000 China)
出处 《锦州医科大学学报》 CAS 2024年第3期19-24,共6页 Journal of Jinzhou Medical University
关键词 小檗碱 脑缺血再灌注 TLR4/p38MAPK信号通路 炎症因子 berberine cerebral ischemia-reperfusion TLR4/p38MAPK signaling pathway inflammatory factors
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