Department of Nutrition and Food Hygiene, Capital Medical University, Beijing, PR China.
Neurosci Lett. 2012 Jan 11;506(2):266-70. doi: 10.1016/j.neulet.2011.11.020. Epub 2011 Nov 23.
Pattern recognition receptors (PRRs) play important roles in the inflammatory responses to Alzheimer's disease (AD). Our previous study indicated that soybean isoflavone (SIF) exhibited anti-inflammatory effect in rats treated by β-amyloid peptides1-42 (Aβ1-42). In present study, we further detected the effects of SIF against inflammation caused by Aβ1-42 treatment in rats. Serum inflammatory mediators and neurotrophic factors including transforming growth factor-β (TGF-β), inducible nitric oxide synthase (iNOS), brain-derived neurotrophic factor (BDNF) and S100β were detected by enzyme-like immunosorbent assay (ELISA). Reverse transcription-polymerase chain reaction (RT-PCR) and western blot methods were applied for detecting mRNA and protein expression of interleukin-1β (IL-1β), iNOS, tumor necrosis factor-α (TNF-α), TGF-β, BDNF, S100β, myeloid differentiation factor88 (Myd88), Toll-like receptor2 (TLR2), formyl peptide receptors (FPRs), inhibitor κB kinase (IKK) and inhibitor κB-α (IκB-α) in rat's brain tissue. Our results indicated that SIF could reduce the production of IL-1β, TNF-α and iNOS induced by Aβ1-42 in serum and brain of rats. SIF also significantly reversed Aβ1-42-induced up-regulation of TLR2, FPR, Myd88, IKK and decreased IκB-α mRNA and protein expressions in rats. These results suggested that TLR2 and FPR might involve in the inflammatory process induced by Aβ1-42 treatment, and SIF was an efficiency compound in reversing the inflammation caused by Aβ1-42 treatment.
模式识别受体 (PRRs) 在阿尔茨海默病 (AD) 的炎症反应中发挥重要作用。我们之前的研究表明,大豆异黄酮 (SIF) 在β-淀粉样肽 1-42 (Aβ1-42) 处理的大鼠中表现出抗炎作用。在本研究中,我们进一步检测了 SIF 对 Aβ1-42 处理大鼠炎症的影响。通过酶联免疫吸附试验 (ELISA) 检测血清炎症介质和神经营养因子,包括转化生长因子-β (TGF-β)、诱导型一氧化氮合酶 (iNOS)、脑源性神经营养因子 (BDNF) 和 S100β。采用逆转录-聚合酶链反应 (RT-PCR) 和 Western blot 方法检测大鼠脑组织中白细胞介素-1β (IL-1β)、iNOS、肿瘤坏死因子-α (TNF-α)、TGF-β、BDNF、S100β、髓样分化因子 88 (Myd88)、Toll 样受体 2 (TLR2)、甲酰肽受体 (FPRs)、抑制剂 κB 激酶 (IKK) 和抑制剂 κB-α (IκB-α) 的 mRNA 和蛋白表达。结果表明,SIF 可降低 Aβ1-42 诱导的大鼠血清和脑组织中 IL-1β、TNF-α 和 iNOS 的产生。SIF 还显著逆转了 Aβ1-42 诱导的 TLR2、FPR、Myd88、IKK 上调和 IκB-α 表达降低。这些结果表明 TLR2 和 FPR 可能参与了 Aβ1-42 处理引起的炎症过程,SIF 是一种有效逆转 Aβ1-42 处理引起的炎症的化合物。