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作 者:谭敏[1] 王宪庆[1] 陈靖[1] 曹浪 沈华[1] 谭旭 王磊 TAN Min;WANG Xianqing;CHEN Jing;CAO Lang;SHEN Hua;TAN Xu;WANG Lei(Department of Pharmacy,Changde Vocational Technical College,Changde 415000,China;Department of Pharmacy,Changsha Central Hospital,Changsha 410006,China)
机构地区:[1]常德职业技术学院药学系,湖南常德415000 [2]长沙市中心医院药学部,湖南长沙410006
出 处:《现代中药研究与实践》2023年第6期34-38,共5页Research and Practice on Chinese Medicines
基 金:湖南省教育厅科学研究项目(21C0953)。
摘 要:目的探讨川陈皮素(Nobiletin,NOB)通过调控PI3K/AKT信号通路抑制心肌肥大的分子机制。方法在培养的H9C2心肌细胞中,建立PE诱导的心肌细胞肥大模型,给予NOB处理,采用qRT-PCR检测心肌肥大相关标记物ANF、BNP、β-MHC的mRNA表达水平,利用免疫荧光检测H9C2心肌细胞表面积,并用Western Blotting的方法检测PI3K、AKT蛋白的表达。结果与对照组相比,PE处理过的H9C2心肌细胞肥大基因显著激活,心肌表面积增大;NOB处理后可抑制PE诱导的肥大基因激活和心肌表面积增大。此外,Western Blotting结果显示,PE处理过的H9C2心肌细胞p-PI3K、p-AKT表达水平下降(P<0.05),NOB治疗后的H9C2心肌细胞p-PI3K/PI3K和p-AKT/AKT水平明显升高(P<0.05)。结论NOB可抑制PE诱导的心肌细胞肥大,其机制可能是通过调控PI3K/AKT信号通路实现的。Objective To explore the molecular mechanism by which Nobiletin(NOB)inhibits myocardial hypertrophy through the modulation of the PI3K/AKT signaling pathway.Methods In cultured H9C2 cardiomyocytes,a PE-induced cardiac hypertrophy model was established.Treatment with NOB was administered.qRT-PCR was used to detect the mRNA expression levels of cardiac hypertrophy-related markers ANF,BNP and β-MHC.Immunofluorescence was employed to measure the surface area of H9C2 cardiomyocytes,and Western Blotting analysis was utilized to examine the protein expression of PI3K and AKT.Results Compared to the control group,PE-treated H9C2 cardiomyocytes exhibited significant activation of hypertrophic genes and increased cardiomyocyte surface area.Treatment with NOB suppressed the activation of hypertrophic genes induced by PE and reduced the increase in cardiomyocyte surface area.Additionally,Western Blotting results demonstrated that the expression levels of p-PI3K and p-AKT in PE-treated H9C2 cardiomyocytes decreased(P<0.05),while the levels of p-PI3K/PI3K and p-AKT/AKT significantly increased after NOB treatment(P<0.05).Conclusion NOB can inhibit PE-induced cardiomyocyte hypertrophy,and this mechanism is achieved through the modulation of the PI3K/AKT signaling pathway.
关 键 词:川陈皮素 PI3K/AKT信号通路 心肌肥大 H9C2心肌细胞
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