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作 者:宋莹 樊荣[1] SONG Ying;FAN Rong(Shaanxi Provincial Baoji Maternal and Child Health Hospital,Baoji 721000)
机构地区:[1]陕西省宝鸡市妇幼保健院,陕西宝鸡721000
出 处:《湖北中医药大学学报》2024年第5期14-17,共4页Journal of Hubei University of Chinese Medicine
基 金:陕西省宝鸡市卫生健康委员会资助项目(项目编号:2021-GJ-LC021)。
摘 要:目的观察积雪草苷对白三烯(LTs)诱导的气管平滑肌细胞(HASMC)增殖、收缩、炎症因子分泌的影响及作用机制。方法将HASMC分为:对照组、模型组、积雪草苷低、中、高剂量组,激活剂组。检测各组细胞增殖、收缩情况及炎症因子水平。结果与对照组比较,模型组HASMC细胞的吸光度(OD490值)、5-乙炔基-2'-脱氧尿嘧啶核苷(EdU)阳性率、增殖细胞核抗原(PCNA)、瞬时受体电位多囊蛋白2(TRPP2)、Toll样受体4(TLR4)、磷酸化核转录因子-κB(p-NF-κB p65)/NF-κB p65、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)水平明显升高,胶原收缩相对面积比值明显降低(P<0.05);与模型组比较,积雪草苷低、中、高剂量组胶原收缩相对面积比值增高,OD490值、EdU阳性率、PCNA、TRPP2、TLR4、p-NF-κB p65/NF-κB p65、IL-1β、IL-6、TNF-α表达水平明显降低;与积雪草苷高剂量组比较,LPS组上述指标变化均显著逆转(P<0.05)。结论积雪草苷通过抑制TLR4/NF-κB信号通路,抑制白三烯诱导的气管平滑肌细胞增殖、收缩、炎症因子分泌。Objective To observe the effect and mechanism of asiaticoside on the proliferation,contraction and inflammatory factor secretion of tracheal smooth muscle cells induced by leukotriene.Methods HASMCs were divided into control group,model group,asiaticoside low,medium and high dose groups,and activator group.Cell proliferation,contraction and inflammatory factor levels were detected in each group.Results Compared with control group,the OD490 value,EdU positive rate,PCNA,TRPP2,TLR4,p-NF-κB p65/NF-κB p65,IL-1β,IL-6 and TNF-α levels of HASMC cells in model group were significantly increased,and the relative area ratio of collagen contraction was significantly decreased(P<0.05);compared with model group,the relative area ratio of collagen contraction in low,medium and high dose groups of asiaticoside was increased,and the OD490 value,EdU positive rate,PCNA,TRPP2,TLR4,p-NF-κB p65/NF-κB p65,IL-1β,IL-6 and TNF-α expression levels were significantly decreased(P<0.05);compared with high-dose asiaticoside group,the changes of the above indexes in LPS group were significantly reversed(P<0.05).Conclusion AS inhibits the proliferation,contraction and secretion of inflammatory factors of tracheal smooth muscle cells induced by leukotriene by inhibiting the TLR4/NF-κB signaling pathway.
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