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作 者:程慧 宋侨 Cheng Hui;Song Qiao(Xiangyang Hospital of Traditional Chinese Medicine,Xiangyang 441000,China)
出 处:《亚太传统医药》2023年第10期22-25,共4页Asia-Pacific Traditional Medicine
基 金:湖北省中医药科研项目(ZY2019F044)。
摘 要:目的:基于TLR4/NF-κB/ICAM-1信号通路表达,探讨桑杏汤对大鼠急性肺损伤作用机制。方法:将40只SPF级雄性SD大鼠,通过脂多糖(LPS)诱导,随机分成空白对照组、模型组、桑杏汤组、甲泼尼龙组,每组10只,建立大鼠急性肺损伤模型。各组鼠肺组织病理变化以HE染色切片作比较;对外周血清炎性因子白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)水平进行ELISA检测;通过Western Blot和RT-PCR法检测TLR4、核转录因子-κB(NF-κB)和抗细胞间黏附的分子-1(ICAM-1)蛋白以及肺组织中的MRNA表达。结果:模型组大鼠支气管黏膜与空白对照组相比,炎症浸润明显,上皮细胞病灶明显增多;桑杏汤组大鼠血清中炎性因子IL-1β、IL-6、TNF-α含量较模型组显著下降(P<0.05,P<0.01);与模型组相比,桑杏汤组大鼠肺组织中的TLR4、NF-κB和ICAM-1蛋白和MRNA表达水平明显下降(P<0.05,P<0.01)。结论:桑杏汤可有效改善大鼠肺组织炎性浸润,可能与减少炎性介质的释放,抑制TLR4/NF-κB/ICAM-1信号通路表达有关。Objective:Based on the expression of TLR4/NF-kB/ICAM-1 signaling pathway,the mechanism of Sangxing Decoction on acute lung injury in rats was explored.Methods:40 SPF male SD rats were randomly divided into control group,model group,Sangxing Decoction group,methylprednisolone group,10 rats in each group,and were induced by lipopolysaccharide(LPS)to establish rats.Acute lung injury model.HE staining sections were used to compare the pathological changes of lung tissues in each group;the inflammatory factors interleukin-1β(IL-1β),interleukin-6(IL-6),tumor necrosis factor-α(TNF-α)in peripheral serum were detected by Elisa method level;Western blot and RT-PCR methods were used to detect the protein and mRNA expressions of Toll-like receptor TLR4,nuclear transcriptionfactorκB(NF-κB)and anti-intercellular adhesion molecule-1(ICAM-1)in lung tissue.Results:Compared with the control group,the tracheobronchial mucosal inflammatory infiltration and epithelial cell lesions of the rats in the model group were significantly changed;Compared with the model group,the expression levels of TLR4,NF-κB and ICAM-1 protein and mRNA in the lung tissue of the Sangxing decoction group were significantly decreased(P<0.05,P<0.01).Conclusion:Sangxing Decoction can effectively improve the inflammatory infiltration of lung tissue,which may be related to reducing the release of inflammatory mediators and inhibiting the expression of TLR4/NF-kB/ICAM-1 signaling pathway.
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