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首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >Anti-inflammatory effects of kolaviron modulate the expressions of inflammatory marker genes, inhibit transcription factors ERK1/2, p-JNK, NF-kappa B, and activate Akt expressions in the 93RS2 Sertoli cell lines
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Anti-inflammatory effects of kolaviron modulate the expressions of inflammatory marker genes, inhibit transcription factors ERK1/2, p-JNK, NF-kappa B, and activate Akt expressions in the 93RS2 Sertoli cell lines

机译:甲钴铁的抗炎作用可调节炎症标记基因的表达,抑制转录因子ERK1 / 2,p-JNK,NF-κB并激活93RS2 Sertoli细胞系中的Akt表达

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摘要

The anti-inflammatory effects of kolaviron (Kol-v) have been demonstrated in several experimental models. The ability of Kol-v to modulate the expressions of inflammatory genes in lipopolysaccharide (LPS)-stimulated Sertoli cell line, 93RS2 was investigated in this study. Kol-v decreased the expressions of inflammatory genes TNF-alpha, Tlr-4, and Nf kappa b1 and has synergistic effect on LPS-induced COX-2 and iNOS expressions at high concentrations (25-100 mu M). At lower concentrations (5-15 mu M), the expressions of TNF-alpha, IL-6, and IL-1 alpha were down-regulated by Kol-v except Tgf beta 1 that was up-regulated. The LPS-induced decrease in the expression of the anti-inflammatory genes IL-3, IL-4, and IL-10 was blocked by Kol-v at all concentrations of Kol-v tested. The LPS-induced phosphorylations of mitogen-activated protein kinase family members (ERK1/2, and p-JNK), decreased I kappa B alpha expression, and decreased Akt phosphorylation was blocked by Kol-v. Our results highlight the potential for Kol-v at lower concentration to ameliorate cellular damage caused by local inflammation.
机译:在几个实验模型中已经证明了克拉维铁(Kol-v)的抗炎作用。在这项研究中,研究了Kol-v调节脂多糖(LPS)刺激的Sertoli细胞系93RS2中炎性基因表达的能力。 Kol-v降低了炎症基因TNF-alpha,Tlr-4和Nf kappa b1的表达,并在高浓度(25-100μM)下对LPS诱导的COX-2和iNOS表达具有协同作用。在较低的浓度(5-15μM)下,除了Tgf beta 1上调外,Kol-v下调了TNF-α,IL-6和IL-1α的表达。在所有测试的Kol-v浓度下,LPS诱导的抗炎基因IL-3,IL-4和IL-10的表达降低均被Kol-v阻止。 LPS诱导的有丝分裂原激活的蛋白激酶家族成员(ERK1 / 2和p-JNK)的磷酸化,降低了IκBα的表达,并降低了Akt的磷酸化被Kol-v阻断。我们的结果强调了低浓度Kol-v改善由局部炎症引起的细胞损伤的潜力。

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