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>The anti-inflammatory effect of kaempferol in aged kidney tissues: the involvement of nuclear factor-kappaB via nuclear factor-inducing kinase/IkappaB kinase and mitogen-activated protein kinase pathways.
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The anti-inflammatory effect of kaempferol in aged kidney tissues: the involvement of nuclear factor-kappaB via nuclear factor-inducing kinase/IkappaB kinase and mitogen-activated protein kinase pathways.
Kaempferol, one of the phytoestrogens, is found in berries and Brassica and Allium species and is known to have antioxidative and anti-inflammatory properties. In the present study, we examined the molecular mechanisms underlying the anti-inflammation effect of kaempferol in an aged animal model. To examine the effect of kaempferol in aged Sprague-Dawley rats, kaempferol was fed at 2 or 4 mg/kg/day for 10 days. The data show that kaempferol exhibited the ability to maintain redox balance. Kaempferol suppressed nuclear factor-kappaB (NF-kappaB) activation and expression of its target genes cyclooxygenase-2, inducible nitric oxide synthase, monocyte chemoattractant protein-1, and regulated upon activation, and normal T-cell expressed and secreted in aged rat kidney and in tert-butylhydroperoxide-induced YPEN-1 cells. Furthermore, kaempferol suppressed the increase of the pro-inflammatory NF-kappaB cascade through modulation of nuclear factor-inducing kinase (NIK)/IkappaB kinase (IKK) and mitogen-activated protein kinases (MAPKs) in aged rat kidney. Based on these results, we concluded that anti-oxidative kaempferol suppressed the activation of inflammatory NF-kappaB transcription factor through NIK/IKK and MAPKs in aged rat kidney.
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机译:山奈酚是植物雌激素之一,存在于浆果、芸苔属和葱属植物中,已知具有抗氧化和抗炎特性。在本研究中,我们研究了山奈酚在老年动物模型中抗炎作用的分子机制。为了检查山奈酚对老年Sprague-Dawley大鼠的影响,山奈酚以2或4mg / kg /天的剂量喂养10天。数据显示,山奈酚表现出维持氧化还原平衡的能力。山奈酚抑制核因子-κB(NF-κB)的激活和靶基因环氧合酶-2、诱导型一氧化氮合酶、单核细胞趋化蛋白-1的表达,并在激活时调节,并在老年大鼠肾脏和叔丁基氢过氧化物诱导的YPEN-1细胞中表达和分泌正常T细胞。此外,山奈酚通过调节老年大鼠肾脏中核因子诱导激酶(NIK)/IkappaB激酶(IKK)和丝裂原活化蛋白激酶(MAPKs)来抑制促炎NF-κB级联反应的增加。基于这些结果,我们得出结论,抗氧化山奈酚通过NIK/IKKs和MAPKs抑制了老年大鼠肾脏中炎症性NF-κB转录因子的激活。
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