This investigation evaluated the neuroprotective effect of melodinhenine B in a cerebral ischemia/reperfusion (I/R)-induced neuronal injury rat model. The effect of melodinhenine B was determined by evaluating the neurological deficit score, cerebral infarcted area, and blood-brain barrier (BBB) permeability. Moreover, the level of inflammatory cytokines and expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κβ), interleukin-1β (IL-1β), NLRP3, zonula occludens-1 (ZO-1), and occluding proteins were estimated by Western blotting. Histopathological changes and immunohistochemical analysis were performed to estimate the effect of melodinhenine B on neuronal injury. The neurological deficit score, percentage of infarcted area, and BBB permeability were improved in the melodinhenine B-treated group of rats. Treatment with melodinhenine B attenuated the altered expression of NF-κβ, IL-1β, NLRP3, ZO-1, and occluding proteins in the brain tissue of I/R-induced neuronal injury rats. The inflammatory cytokine levels were reduced in the melodinhenine B-treated group. Histopathologically, melodinhenine B reversed the pathological changes in the brain tissues of I/R-induced neuronal injury rats. In conclusion, melodinhenine B protects against neuronal injury in cerebral ischemia-reperfusion injury rats by regulating the inflammasomes.

中文翻译：

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Melodinhenine B减弱在脑缺血/再灌注诱导的神经元损伤大鼠模型中NLRP3的表达。

这项研究评估了美洛地宁碱B在脑缺血/再灌注（I / R）诱导的神经元损伤大鼠模型中的神经保护作用。通过评估神经功能缺损评分，脑梗死面积和血脑屏障（BBB）通透性来确定美洛地宁B的作用。此外，活化的B细胞（NF-κβ），白介素-1β（IL-1β），NLRP3，闭合小带-1（ZO-1）的炎症细胞因子水平和核因子κ轻链增强子的表达，通过蛋白质印迹法估计蛋白质的结合。进行了组织病理学改变和免疫组织化学分析，以评估美洛地宁B对神经元损伤的影响。美洛地宁碱B处理组大鼠的神经功能缺损评分，梗塞面积百分比和BBB通透性均得到改善。在我/ R诱导的神经元损伤大鼠的脑组织中，用美洛地宁碱B处理可减轻NF-κβ，IL-1β，NLRP3，ZO-1和闭塞蛋白的表达变化。美洛丁宁B治疗组的炎症细胞因子水平降低。在组织病理学上，美洛地宁B逆转了I / R诱导的神经元损伤大鼠脑组织的病理变化。总之，美洛地宁B可以通过调节炎症小体来预防脑缺血再灌注损伤大鼠的神经元损伤。麦洛地宁B逆转了I / R诱导的神经元损伤大鼠脑组织的病理变化。总之，美洛地宁B可以通过调节炎症小体来预防脑缺血再灌注损伤大鼠的神经元损伤。麦洛地宁B逆转了I / R诱导的神经元损伤大鼠脑组织的病理变化。总之，美洛地宁B可以通过调节炎症小体来预防脑缺血再灌注损伤大鼠的神经元损伤。