首页|期刊导航|激光生物学报|儿茶素抑制p38 MAPK磷酸化减轻脂多糖诱导的大鼠心肌细胞凋亡、炎症及氧化损伤

儿茶素抑制p38 MAPK磷酸化减轻脂多糖诱导的大鼠心肌细胞凋亡、炎症及氧化损伤OACSTPCD

Catechin Alleviates Apoptosis,Inflammation and Oxidative Damage of Rat Cardiomyocytes Induced by Lipopolysaccharide by Inhibiting p38 MAPK Phosphorylation

中文摘要英文摘要

为了研究儿茶素对脂多糖(LPS)诱导的大鼠心肌细胞(H9C2)氧化损伤、炎症和凋亡的影响以及对p38丝裂原活化蛋白激酶(MAPK)信号通路的调控作用,本研究体外培养H9C2细胞,并将其分为对照组(不做干预处理)、LPS组(10 μg/mL LPS处理)、不同浓度儿茶素组(在LPS组基础上以20、40、80、160 nmol/L儿茶素处理)、SB203580组(10 μg/mL LPS+1 μmol/L SB203580处理)、抑制剂组(10 μg…查看全部>>

To investigate the effects of catechins on oxidative damage,inflammation and apoptosis of rat cardiomyocytes(H9C2)induced by lipopolysaccharide(LPS),as well as the regulation of p38 mitogen-activated protein kinase(MAPK)sig-naling pathway,H9C2 cells were cultured in vitro and divided into the control group which is without intervention,LPS group with 10 μg/mL LPS treatment,catechin with different concentrations(20,40,80,160 nmol/L catechin treatment based on…查看全部>>

邢建华;孙鹿璐;李哲贤

河北中石油中心医院老年医学科,廊坊 065000河北中石油中心医院老年医学科,廊坊 065000河北中石油中心医院老年医学科,廊坊 065000

临床医学

儿茶素心肌细胞脂多糖p38丝裂原活化蛋白激酶信号通路氧化损伤

catechinscardiomyocyteslipopolysaccharidep38 mitogen-activated protein kinase signaling pathwayoxida-tive damage

《激光生物学报》 2024 (3)

259-266,8

10.3969/j.issn.1007-7146.2024.03.009

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