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首页> 外文期刊>The Journal of dermatology >Bidens pilosa suppresses interleukin-1beta-induced cyclooxygenase-2 expression through the inhibition of mitogen activated protein kinases phosphorylation in normal human dermal fibroblasts.
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Bidens pilosa suppresses interleukin-1beta-induced cyclooxygenase-2 expression through the inhibition of mitogen activated protein kinases phosphorylation in normal human dermal fibroblasts.

机译:Bidens pilosa通过抑制正常人皮肤成纤维细胞中有丝分裂原活化蛋白激酶的磷酸化来抑制白介素1β诱导的环氧合酶2表达。

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摘要

Bidens pilosa (BP) Linn. var. radiata is a plant used in traditional folk medicine. It is clinically effective in various diseases; the pathogenesis of most of these involves cyclooxygenase (COX)-2. To investigate the mechanism on which the clinical effectiveness of BP is based, we examined its effects on COX-2 expression and its major product, prostaglandin (PG)E(2), under conditions of inflammation. We induced inflammation in normal human dermal fibroblasts with interleukin (IL)-1beta and examined the effects of BP on COX-2 expression and PGE(2) production using Western blotting and competitive enzyme immunoassay, respectively. The functional involvements of mitogen activated protein kinases (MAPK) ERK1/2, p38, and JNK in COX-2 expression were also examined by Western blotting. IL-1beta-induced COX-2 expression was regulated by MAPK pathways, especially by p38. BP inhibited the phosphorylation of MAPKs, COX-2 expression, and subsequent PGE(2) production. The physiological activities and clinical effectiveness of BP observed under diverse conditions may be partly attributable to its ability to inhibit MAPK, mainly p38, activity, COX-2 expression, and subsequent PGE(2) production.
机译:Bidens pilosa(BP)Linn。变种radiata是用于传统民间医学的植物。在多种疾病上具有临床疗效;其中大多数的发病机制都涉及环氧合酶(COX)-2。为了研究BP的临床有效性所基于的机制,我们研究了其在炎症条件下对COX-2表达及其主要产物前列腺素(PG)E(2)的影响。我们用白介素(IL)-1beta诱导正常人真皮成纤维细胞发炎,并分别使用Western印迹法和竞争酶免疫法检测了BP对COX-2表达和PGE(2)产生的影响。还通过蛋白质印迹法检查了有丝分裂原活化蛋白激酶(MAPK)ERK1 / 2,p38和JNK在COX-2表达中的功能参与。 IL-1β诱导的COX-2表达受MAPK途径,尤其是p38的调节。 BP抑制MAPKs,COX-2表达和随后的PGE(2)生产的磷酸化。在不同条件下观察到的BP的生理活性和临床有效性可能部分归因于其抑制MAPK的能力,主要是p38,活性,COX-2表达和随后的PGE(2)产生。

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