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作 者:姚明言[1] 张靖[2] 郭淑芹[1] 宋茜茜 徐帅妹 YAO Mingyan;ZHANG Jing;GUO Shuqin(Department of Endocrinology,Baoding No.1 Central Hospital,Baoding 071000,China)
机构地区:[1]保定市第一中心医院内分泌科,071000 [2]河北大学附属医院心内科 [3]南方医科大学口腔医院牙体牙髓科
出 处:《中国糖尿病杂志》2024年第1期46-50,共5页Chinese Journal of Diabetes
基 金:河北省自然科学基金资助项目(H2023104011);河北省医学科学研究课题项目(20241470)。
摘 要:目的探讨利拉鲁肽(Lir)通过抑制高糖环境NOD样受体家族核苷酸结合寡聚化结构域样受体3(NLRP3)炎性体活化保护人髓核细胞(NPCs)的作用及机制。方法培养人髓核细胞株,第三代髓核细胞随机分为对照组(Con组)、高糖组(HG组)、Lir干预组(Lir组),培养48 h。ELISA法检测IL-1β,流式细胞术检测活性氧簇(ROS),Western blot法检测NLRP3、半胱天冬氨酸酶-1前体(Pro-caspase-1)、半胱天冬氨酸酶-1(Caspase-1)蛋白表达。结果与Con组比较,HG、Lir组IL-1β、ROS、NLRP3、Pro-caspase-1、Caspase-1蛋白表达、细胞凋亡率升高(P<0.05)。与HG组比较,Lir组IL-1β、ROS、NLRP3、Pro-caspase-1、Caspase-1蛋白表达、细胞凋亡率降低(P<0.05)。结论Lir通过抑制NLRP3炎性体活化,降低IL-1β分泌,抑制细胞凋亡,保护人NPCs。Objective To evaluate the protective effect of human nucleus pulposus cell by Liraglutide(Lir)under high-glucose environment via inhibition of NOD-like receptor family,pyrin domain containing 3(NLRP3)inflammasome activation and its mechanism.Methods Human nucleus pulposus cell lines were cultured and the third-generation nucleus pulposus cells were randomly divided into control group(Con group),high glucose group(HG group),and Liraglutide interference group(Lir group),and cultured for 48 h.ELISA was used to detect interleukin IL-1β;flow cytometry was used to testreactive oxygen species(ROS),and Western blot was used to evaluate the protein expressions of NLRP3,Pro-caspase-1,and Caspase-1.Results Compared with Con group,IL-1β,ROS,NLRP3,Pro-caspase-1,Caspase-1protein expression and cell apoptosis were increased in HG and Lir groups(P<0.05).Compared with HG group,IL-1β,ROS,NLRP3,Pro-caspase-1,Caspase-1 protein expression and cell apoptosis were significantly decreased in Lir group(P<0.05).Conclusion Liraglutide protects human NPCs by inhibiting the activation of NLRP3 inflammasome,reducing IL-1βsecretion,and inhibiting cell apoptosis.
关 键 词:NOD样受体家族核苷酸结合寡聚化结构域样受体3炎性体 利拉鲁肽 髓核细胞 高糖
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