首页> 外文期刊>Journal of pharmacological sciences. >Anti-inflammatory Activity of Methylene Chloride Fraction From Glehnia littoralis Extract via Suppression of NF-κB and Mitogen-Activated Protein Kinase Activity
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Anti-inflammatory Activity of Methylene Chloride Fraction From Glehnia littoralis Extract via Suppression of NF-κB and Mitogen-Activated Protein Kinase Activity

机译:通过抑制NF-κB和丝裂原激活的蛋白激酶活性,从北沙参提取物中的亚甲酰氯的抗炎活性

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References(42) Cited-By(16) Glehnia littoralis (Umbelliferae) has been used traditionally in Korean, Japanese, and Chinese medicine for the treatment of immune-related diseases; however, its anti-inflammatory activity and underlying mechanism remain to be defined. We investigated the anti-inflammatory effect and inhibitory mechanism on inflammation by the methylene chloride fraction from Glehnia littoralis extract (MCF-GLE), which was more effective than Glehnia littoralis extract (GLE). MCF-GLE inhibited 12-O-Tetradecanoyl-phorbol-13-acetate (TPA)–induced inflammation in an inflammatory edema mouse model. Also, MCF-GLE strongly inhibited the releases of nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) and significantly suppressed the mRNA and protein expression of inducible nitric oxide synthase and cyclooxygenase-2 in lipopolysaccharide-stimulated RAW 264.7 macrophage cells in a dose-dependent manner. Furthermore, MCF-GLE suppressed NF-κB activation and IκB-α degradation. MCF-GLE also attenuated the activation of ERK and JNK in a dose-dependent manner. These results indicate that MCF-GLE has an inhibitory effect on the in vivo and in vitro inflammatory reaction and is a possible therapeutic agent. Our results suggest that the anti-inflammatory properties of MCF-GLE may result from the inhibition of pro-inflammatory mediators, such as NO, PGE2, TNF-α, and IL-1β via suppression of NF-κB– and mitogen-activated protein kinases-dependent pathways.
机译:参考文献(42)被引用的(16)锦鸡儿(Umbelliferae)在韩国,日本和中药中传统上用于治疗免疫相关疾病。然而,其抗炎活性及其潜在机制尚待确定。我们研究了由沙参提取物(MCF-GLE)分离出的二氯甲烷的抗炎作用和抑制炎症的机制,它比沙参提取物(GLE)更有效。 MCF-GLE在炎性水肿小鼠模型中抑制了12-O-十四碳酰基-phorbol-13-乙酸盐(TPA)诱导的炎症。此外,MCF-GLE强烈抑制一氧化氮(NO),前列腺素E2(PGE2),肿瘤坏死因子-α(TNF-α)和白介素-1β(IL-1β)的释放,并显着抑制mRNA和蛋白质表达脂多糖刺激的RAW 264.7巨噬细胞中诱导型一氧化氮合酶和环氧合酶-2的剂量依赖性。此外,MCF-GLE抑制NF-κB活化和IκB-α降解。 MCF-GLE还以剂量依赖的方式减弱ERK和JNK的激活。这些结果表明MCF-GLE对体内和体外炎症反应具有抑制作用,并且是可能的治疗剂。我们的结果表明,MCF-GLE的抗炎特性可能是通过抑制NF-κB和促分裂原活化蛋白而抑制促炎性介质(如NO,PGE2,TNF-α和IL-1β)产生的激酶依赖性途径。

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