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首页> 外文期刊>International Journal of Molecular Sciences >Resveratrol Attenuates Acute Inflammatory Injury in Experimental Subarachnoid Hemorrhage in Rats via Inhibition of TLR4 Pathway
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Resveratrol Attenuates Acute Inflammatory Injury in Experimental Subarachnoid Hemorrhage in Rats via Inhibition of TLR4 Pathway

机译：白藜芦醇通过抑制TLR4途径减轻大鼠实验性蛛网膜下腔出血的急性炎症损伤。

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Toll-like receptor 4 (TLR4) has been proven to play a critical role in neuroinflammation and to represent an important therapeutic target following subarachnoid hemorrhage (SAH). Resveratrol (RSV), a natural occurring polyphenolic compound, has a powerful anti-inflammatory property. However, the underlying molecular mechanisms of RSV in protecting against early brain injury (EBI) after SAH remain obscure. The purpose of this study was to investigate the effects of RSV on the TLR4-related inflammatory signaling pathway and EBI in rats after SAH. A prechiasmatic cistern SAH model was used in our experiment. The expressions of TLR4, high-mobility group box 1 (HMGB1), myeloid differentiation factor 88 (MyD88), and nuclear factor-κB (NF-κB) were evaluated by Western blot and immunohistochemistry. The expressions of Iba-1 and pro-inflammatory cytokines in brain cortex were determined by Western blot, immunofluorescence staining, or enzyme-linked immunosorbent assay. Neural apoptosis, brain edema, and neurological function were further evaluated to investigate the development of EBI. We found that post-SAH treatment with RSV could markedly inhibit the expressions of TLR4, HMGB1, MyD88, and NF-κB. Meanwhile, RSV significantly reduced microglia activation, as well as inflammatory cytokines leading to the amelioration of neural apoptosis, brain edema, and neurological behavior impairment at 24 h after SAH. However, RSV treatment failed to alleviate brain edema and neurological deficits at 72 h after SAH. These results indicated that RSV treatment could alleviate EBI after SAH, at least in part, via inhibition of TLR4-mediated inflammatory signaling pathway.
机译：已证明Toll样受体4（TLR4）在神经炎症中起关键作用，并代表蛛网膜下腔出血（SAH）后的重要治疗靶标。白藜芦醇（RSV）是一种天然的多酚化合物，具有强大的抗炎特性。但是，RSV预防SAH后早期脑损伤（EBI）的潜在分子机制仍然不清楚。这项研究的目的是调查SAH后RSV对TLR4相关的炎症信号通路和EBI的影响。在我们的实验中使用了前交叉型水箱SAH模型。用Western blot和免疫组化方法检测TLR4，高迁移率族框1（HMGB1），骨髓分化因子88（MyD88）和核因子-κB（NF-κB）的表达。通过蛋白质印迹，免疫荧光染色或酶联免疫吸附试验确定脑皮层中Iba-1和促炎细胞因子的表达。进一步评估神经细胞凋亡，脑水肿和神经功能，以研究EBI的发展。我们发现用SAV治疗SAH后可以显着抑制TLR4，HMGB1，MyD88和NF-κB的表达。同时，在SAH后24小时，RSV显着降低了小胶质细胞的活化以及炎症细胞因子，从而改善了神经细胞凋亡，脑水肿和神经行为受损。然而，在SAH后72小时，RSV治疗未能减轻脑水肿和神经功能缺损。这些结果表明RSV治疗可以至少部分地通过抑制TLR4介导的炎性信号通路来减轻SAH后的EBI。

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