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作 者:李慎富 朱付平[2] 黄泓珺 LI Shenfu;ZHU Fuping;HUANG Hongjun(Hunan University of Traditional Chinese Medicine,Changsha 410208,China)
机构地区:[1]湖南中医药大学,湖南长沙410208 [2]湖南中医药大学第一附属医院,湖南长沙410021
出 处:《陕西中医》2024年第12期1592-1597,共6页Shaanxi Journal of Traditional Chinese Medicine
基 金:国家自然科学基金资助项目(82274541);湖南省自然科学基金资助项目(2020JJ4070)。
摘 要:目的:基于miR-675/NF-κB信号通路研究桃红四物汤对肢体缺血再灌注损伤炎症反应的影响。方法:78只大鼠分为四组,除正常对照组外,其余三组均复制缺血再灌注损伤模型。于再灌注0、2、4、8 h四个时间点取材骨骼肌,HE染色观察骨骼肌形态;TUNEL荧光染色观察骨骼肌细胞凋亡情况;RT-qPCR检测miR-675-5p、NF-κB p65、p50表达;Western blot检测NF-κB p65、p50蛋白表达;ELISA检测血清TNF-α、IL-1β、IL-6水平。结果:与模型组相比,桃红四物汤组、miR-675阻滞剂组血清TNF-α、IL-1β、IL-6水平降低(均P<0.05);桃红四物汤、miR-675阻滞剂干预,可保护骨骼肌细胞,减轻凋亡程度,与模型组相比,可降低NF-κB p65、p50的表达(均P<0.05)。结论:桃红四物汤可通过减轻炎症反应保护骨骼肌细胞,这一过程可能与miR-675/NF-κB信号通路的激活有关。Objective:To study the effect of Taohong Siwu decoction on inflammatory response of limb ischemia-reperfusion injury based on miR-675/NF-κB signaling pathway.Methods:Seventy-eight rats were divided into four groups.Except for the normal control group,the other three groups were replicated for ischemia-reperfusion injury,and then skeletal muscle was taken at four time points of 0,2,4 and 8 hours.HE staining was used to observe the morphology of skeletal muscle.The apoptosis of skeletal muscle cells was observed by TUNEL fluorescence staining.RT-qPCR was used to detect the expression of miR-675-5p and NF-κB p65,p50 in cells.The expression of NF-κB p65,p50 in cells was detected by Western blot.The concentrations of TNF-α,IL-1βand IL-6 in serum were quantified by ELISA.Results:Compared with the model group,the levels of serum TNF-α,IL-1βand IL-6 in the Taohong Siwu decoction and miR-675 inhibitor groups were significantly lower(all P<0.05).Under the intervention of Taohong Siwu decoction and miR-675 inhibitor,it can protect skeletal muscle cells and reduce the degree of apoptosis.Compared with the model group,it can also reduce the expression of NF-κB p65,p50(all P<0.05).Conclusion:Taohong Siwu decoction can protect skeletal muscle cells by reducing inflammatory response,which may be related to the activation of miR-675/NF-κB signaling pathway.
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