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发酵人参通过抑制 NF-κB 对链脲佐菌素诱导的胰岛 β 细胞损伤的保护作用。

Protective effects of fermented ginseng on streptozotocin-induced pancreatic beta-cell damage through inhibition of NF-kappaB.

机构信息

Department of Life and Nanopharmaceutical Science, College of Pharmacy, Kyung Hee University, Seoul 130-701, Korea.

出版信息

Int J Mol Med. 2010 Jan;25(1):53-8.

PMID:19956901
Abstract

Ginseng (Panax ginseng C.A. Meyer) is widely used in Asian countries as a traditional medicine for the treatment of various diseases. It is known to have anti-inflammatory effects, although the mechanism is not clear. In this study, preventive effects of fermented ginseng (FG) against streptozotocin (STZ)-induced pancreatic beta-cell death was assessed in RINm5F insulinoma cells. FG markedly inhibited the production of nitrite in a dose-dependent manner. The decrease in nitrite production was found to correlate with reduced inducible nitric oxide (iNOS) protein and mRNA levels. To characterize the anti-inflammatory mechanism of FG at the transcriptional level, we examined effects of FG on the activity of nuclear factor-kappaB (NF-kappaB). FG reduced a translocation of the NF-kappaB subunit and NF-kappaB-dependent transcriptional activity. FG blocked signaling upstream of NF-kappaB activation, such as degradation of inhibitor factor-kappaBalpha (IkappaBalpha ) and phosphorylations of extracellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK). These results suggest that FG protects against STZ-induced pancreatic beta-cell damage by downregulation of iNOS, cyclooxygenase-2 (COX-2), and tumor necrosis factor-alpha (TNF-alpha ) gene expressions by blocking NF-kappaB and mitogen-activated protein kinase activities.

摘要

人参(Panax ginseng C.A. Meyer)在亚洲国家被广泛用作传统药物,用于治疗各种疾病。已知其具有抗炎作用,但其机制尚不清楚。在这项研究中,评估了发酵人参(FG)对链脲佐菌素(STZ)诱导的胰岛β细胞死亡的预防作用。FG 呈剂量依赖性显著抑制亚硝酸盐的产生。发现亚硝酸盐产量的减少与诱导型一氧化氮合酶(iNOS)蛋白和 mRNA 水平的降低相关。为了在转录水平上表征 FG 的抗炎机制,我们研究了 FG 对核因子-κB(NF-κB)活性的影响。FG 减少了 NF-κB 亚基的易位和 NF-κB 依赖性转录活性。FG 阻断了 NF-κB 激活的上游信号,如抑制剂κBα(IkappaBalpha)的降解和细胞外信号调节激酶(ERK)和 c-Jun NH2-末端激酶(JNK)的磷酸化。这些结果表明,FG 通过阻断 NF-κB 和丝裂原活化蛋白激酶的活性,下调 iNOS、环加氧酶-2(COX-2)和肿瘤坏死因子-α(TNF-α)基因的表达,从而防止 STZ 诱导的胰岛β细胞损伤。

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