首页> 外文期刊>Phytotherapy research: PTR >Houttuynia cordata Thunb. Volatile oil exhibited anti-inflammatory effects in vivo and inhibited nitric oxide and tumor necrosis factor-α production in LPS-stimulated mouse peritoneal macrophages in vitro
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Houttuynia cordata Thunb. Volatile oil exhibited anti-inflammatory effects in vivo and inhibited nitric oxide and tumor necrosis factor-α production in LPS-stimulated mouse peritoneal macrophages in vitro

机译:鱼腥草。挥发油在体内表现出抗炎作用,并在体外脂多糖刺激的小鼠腹膜巨噬细胞中抑制一氧化氮和肿瘤坏死因子-α的产生

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Houttuynia cordata Thunb. (HC) is a medicinal herb that generally used in traditional Chinese medicine for treating allergic inflammation. The present study investigated the inhibitory effect of the volatile oil from HC Thunb. on animal models of inflammation and the production of inflammatory mediators in vivo and in vitro. In vivo, xylene-induced mouse ear edema, formaldehyde-induced paw edema and carrageenan-induced mice paw edema were significantly decreased by HC volatile oil. HC volatile oil showed pronounced inhibition of prostaglandin (PG) E_2 and malondialdehyde production in the edematous exudates. In vitro exposure of mouse resident peritoneal macrophages to 1, 10, 100 and 1000 μg/mL of HC volatile oil significantly suppressed lipopolysaccharide (LPS)-stimulated production of NO and tumor necrosis factor-α (TNF-α) in a dose-dependent manner. Exposure to HC volatile oil had no effect on cell viability and systemic toxicity. Furthermore, HC volatile oil inhibited the production of NO and TNF-α by down-regulating LPS-stimulated iNOS and TNF-α mRNA expression. Western blot analysis showed that HC volatile oil attenuated LPS-stimulated synthesis of iNOS and TNF-α protein in the macrophages, in parallel. These findings add a novel aspect to the biological profile of HC and clarify its anti-inflammatory mechanism.
机译:鱼腥草。 HC(HC)是一种中草药,通常用于治疗过敏性炎症。本研究调查了HC Thunb挥发油的抑制作用。体内和体外炎症动物模型和炎症介质的产生。在体内,HC挥发油可显着降低二甲苯诱导的小鼠耳朵水肿,甲醛诱导的爪水肿和角叉菜胶诱导的小鼠爪水肿。 HC挥发油在水肿渗出物中显示出对前列腺素(PG)E_2和丙二醛产生的明显抑制作用。小鼠常驻腹膜巨噬细胞在1、10、100和1000μg/ mL HC挥发油中的体外暴露以剂量依赖性方式显着抑制脂多糖(LPS)刺激的NO和肿瘤坏死因子-α(TNF-α)的产生方式。暴露于HC挥发油对细胞活力和全身毒性没有影响。此外,HC挥发油通过下调LPS刺激的iNOS和TNF-αmRNA表达来抑制NO和TNF-α的产生。 Western印迹分析表明,HC挥发油平行地减弱了巨噬细胞中LPS刺激的iNOS和TNF-α蛋白的合成。这些发现为HC的生物学特性增加了一个新的方面,并阐明了其抗炎机制。

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