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Polysaccharide extracts of iCirsium japonicum/i protect rat H9c2 myocardial cells from oxidative stress induced by hydrogen peroxide

机译:日本毛C多糖提取物可保护大鼠H9c2心肌细胞免受过氧化氢诱导的氧化应激的影响

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Highlights The current study found that the polysaccharide extract of Daji (Cirsium japonicum) have a favorable therapeutic effect against oxidative stress and the underlying mechanism might be involved with MAPK pathway. Editor’s Summary Daji (Cirsium japonicum) have been traditionally utilized by the Tibetan and Mongolian people since the Tang Dynasty of China (618 A.D. - 907 A.D.). Daji (Cirsium japonicum) has been applied against gastric disorders, lung diseases, and cardiovascular problems in the traditional Chinese medicinal system. The present study was to investigate the protective effects of Daji (Cirsium japonicum) polysaccharide extracts (CJP) against hydrogen peroxide (H2O2) shock in rat H9c2 myocardial cells. First, CJP was isolated by hot water extraction and ethanol precipitation; it was then characterized by high performance liquid chromatography and infrared spectrum analysis. Rat H9c2 cells were subjected to H2O2 treatment to establish a cell injury model. The 3- (4,5- dimethylthiazol- 2-yl)-2,5- diphenyltetrazolium bromide assay showed that CJP pretreatment significantly ameliorated the H2O2 injury in a dose-dependent manner. Furthermore, the cell apoptosis induced by H2O2 was markedly inhibited by CJP pretreatment, whereas the cleavage level of caspase-3, -8, and -9 was reduced. In addition, the p38 mitogen-activated protein kinase pathway might be involved in the protective effect of CJP on myocardial cells. Therefore, we conclude that polysaccharide extracts of Daji (Cirsium japonicum) protect rat H9c2 myocardial cells from oxidative stress induced by H2O2.
机译:要点当前的研究发现,大吉多糖提取物对氧化应激具有良好的治疗作用,其潜在机制可能与MAPK通路有关。编辑摘要自唐朝(公元618年至907年)以来,藏族和蒙古族人就一直使用大吉(Cirsium japonicum)。大吉(Cirsium japonicum)已在传统中药系统中用于治疗胃部疾病,肺部疾病和心血管疾病。本研究旨在研究大蓟(Cirsium japonicum)多糖提取物(CJP)对大鼠H9c2心肌细胞中过氧化氢(H2O2)休克的保护作用。首先,通过热水萃取和乙醇沉淀分离出CJP。然后通过高效液相色谱和红外光谱分析对其进行表征。对大鼠H9c2细胞进行H2O2处理,以建立细胞损伤模型。 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物测定表明,CJP预处理以剂量依赖性方式显着改善了H2O2损伤。此外,H2O2诱导的细胞凋亡被CJP预处理显着抑制,而caspase-3,-8和-9的裂解水平降低。此外,p38丝裂原激活的蛋白激酶途径可能参与了CJP对心肌细胞的保护作用。因此,我们得出结论,大蓟多糖提取物可以保护大鼠H9c2心肌细胞免受H2O2诱导的氧化应激。

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