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首页> 外文期刊>Drug Design, Development and Therapy >Rutaecarpine may improve neuronal injury, inhibits apoptosis, inflammation and oxidative stress by regulating the expression of ERK1/2 and Nrf2/HO-1 pathway in rats with cerebral ischemia-reperfusion injury
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Rutaecarpine may improve neuronal injury, inhibits apoptosis, inflammation and oxidative stress by regulating the expression of ERK1/2 and Nrf2/HO-1 pathway in rats with cerebral ischemia-reperfusion injury

机译：Rutaecarpine可能通过调节脑缺血再灌注损伤大鼠的ERK1 / 2和Nrf2 / HO-1通路表达来改善神经元损伤，抑制细胞凋亡，炎症和氧化应激

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Background: Cerebral ischemia-reperfusion (CI/R) injury is a more serious brain injury caused by the recovery of blood supply after cerebral ischemia for a certain period of time. Rutaecarpine (Rut) is an alkaloid isolated from Evodia officinalis with various biological activities. Previous studies have shown that Rut has a certain protective effect on ischemic brain injury, but the specific molecular mechanism is still unknown. Methods: In this study, a rat model of CI/R was established to explore the effects and potential molecular mechanisms of Rut on CI/R injury in rats. Results: The results showed that Rut alleviated neuronal injury induced by CI/R in a dose-dependent manner. Besides, Rut inhibited neuronal apoptosis by inhibiting the activation of caspase 3 and the expression of Bax. In addition, Rut alleviated the inflammatory response and oxidative stress caused by CI/R through inhibiting the production of pro-inflammatory factors (IL-6 and IL-1β), lactate dehydrogenase (LDH), malondialdehyde (MDA) and ROS, and increased the levels of anti-inflammatory factors (IL-4 and IL-10) and superoxide dismutase (SOD). Biochemically, Western blot analyses showed that Rut inhibited the phosphorylation of ERK1/2 and promoted the expression of nuclear factor-erythroid 2 related factor 2 (Nrf2) pathway-related proteins (Nrf2, heme oxygenase 1 (HO-1) and NAD (P) H-quinone oxidoreductase 1) in a dose-dependent manner. These results show that Rut may alleviate brain injury induced by CI/R by regulating the expression of ERK1/2 and the activation of Nrf2/HO-1 pathway. Conclusion: In conclusion, these results suggest that Rut may be used as an effective therapeutic agent for damage caused by CI/R.
机译：背景：脑缺血再灌注（CI / R）损伤是由脑缺血一定时间后血液供应恢复引起的一种较严重的脑损伤。 Rutaecarpine（Rut）是一种从吴茱vo中提取的生物碱，具有多种生物活性。先前的研究表明，Rut对缺血性脑损伤具有一定的保护作用，但具体的分子机制仍不清楚。方法：本研究建立了CI / R大鼠模型，以探讨Rut对大鼠CI / R损伤的影响及其潜在的分子机制。结果：结果表明，Rut以剂量依赖的方式减轻了CI / R诱导的神经元损伤。此外，Rut通过抑制caspase 3的活化和Bax的表达来抑制神经元的凋亡。此外，Rut通过抑制促炎因子（IL-6和IL-1β），乳酸脱氢酶（LDH），丙二醛（MDA）和ROS的产生，减轻了CI / R引起的炎症反应和氧化应激，并增加了抗炎因子（IL-4和IL-10）和超氧化物歧化酶（SOD）的水平。生化方面，Western印迹分析表明Rut抑制ERK1 / 2的磷酸化并促进核因子-类红细胞2相关因子2（Nrf2）途径相关蛋白（Nrf2，血红素加氧酶1（HO-1）和NAD（P ）H-醌氧化还原酶1）呈剂量依赖性。这些结果表明，Rut可以通过调节ERK1 / 2的表达和Nrf2 / HO-1途径的激活来减轻CI / R诱导的脑损伤。结论：总之，这些结果表明Rut可以用作CI / R引起的损伤的有效治疗剂。

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