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作 者:胡洋 潘韵铮 李庆菊 郑仕中[1] 卞勇[1] 时乐[1] 范方田 蒋宝平[1] 许立[1] HU Yang;PAN Yun-zheng;LI Qing-ju;ZHENG Shi-Zhong;BIAN Yong;SHI Le;FAN Fang-tian;JIANG Bao-ping;XU li(Nanjing University of Traditional College of Pharmacy,Nanjing 210023,China;Nanjing University of Traditional Chinese Medicine Hanlin College,Taizhou,Jiangsu 225300,China)
机构地区:[1]南京中医药大学药学院,江苏南京210023 [2]南京中医药大学翰林学院,江苏泰州225300
出 处:《中国药理学通报》2020年第2期210-215,共6页Chinese Pharmacological Bulletin
基 金:江苏省中医药局科技项目(No ZD301701)。
摘 要:目的探究丹酚酸B(Sal B)能否通过调控NLRP3炎症小体priming阶段减轻缺氧诱导大鼠心肌细胞损伤。方法CCK8法检测不同浓度丹酚酸B对大鼠H9C2细胞生长的影响,并挑选出合适的丹酚酸B实验浓度;微孔板、ELISA法检测缺氧造模后实验组,不同浓度给药组,以及抑制剂组LDH/cTn/IL-1β的分泌水平;qPCR以及蛋白质免疫印迹法检测造模后实验组,不同浓度给药组以及抑制剂组TLR4/Myd88/IRAK1/NF-κB/NLRP3基因以及蛋白表达水平。结果经过缺氧处理后,H9C2细胞活性下降,LDH/cTn/IL-1β分泌量升高,TLR4/Myd88/IRAK1/NF-κB/NLRP3在mRNA水平以及蛋白表达上调;与模型组相比,丹酚酸B预处理24h后,H9C2细胞活性增加,LDH/cTn/IL-1β分泌量下降,TLR4/Myd88/IRAK1/NF-κB/NLRP3 mRNA水平以及蛋白表达水平降低。结论丹酚酸B可以通过调控NLRP3炎症小体priming阶段,减轻缺氧诱导的大鼠心肌细胞损伤。Aim To investigate whether Sal B alleviates hypoxic-induced cardiomyocyte injury by regulating the priming of NLRP3 inflammasomes.Methods The effects of Sal B on growth of H9C2 cells were examined by CCK8 assay,then the appropriate concentration of Sal B was selected.The expression level of LDH was detected by Microtiter assay.The expression levels of cTn/IL-1βwere measured by Elisa assay.The protein and mRNA levels of TLR4/Myd88/IRAK1/NF-κB/NLRP3 were detected by Western blot and qPCR.Results Hypoxia intervention notably reduced the viability of H9C2 cells and increased the expression levels of cTn/IL-1β.Besides,the protein and mRNA expression levels of TLR4/Myd88/IRAK1/NF-κB/NLRP3 were significant uP-regulated after hypoxia intervention.However,the viability of H9C2 cells increased,the secretion levels of LDH/cTn/IL-1βwere reduced,and the protein and mRNA levels of TLR4/Myd88/IRAK1/NF-κB/NLRP3 were significant inhibited after pretreated with Sal B.Conclusion Sal B attenuates cardiomyocyte injury by regulating the priming of NLRP3 inflammasome.
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