舒芬太尼通过调节SDF-1/CXCR4信号通路对脑出血大鼠的神经功能的改善作用

Sufentanil improving neurological function in rats with cerebral hemorrhage by regulating SDF-1/CXCR4 signaling pathway

  • 摘要: 目的:探讨舒芬太尼通过调节SDF-1/CXCR4信号通路对脑出血(ICH)大鼠的神经功能恢复的作用及其潜在机制。方法:通过胶原酶诱导建立ICH后的脑损伤模型,将大鼠分为4组:对照组(假手术处理,sham组),ICH模型诱导组(ICH组),ICH+DMSO组(大鼠ICH模型后用DMSO处理),ICH+舒芬太尼组(大鼠ICH模型后用50 mg/kg·d-1的舒芬太尼处理)。利用生物化学分析评估神经严重程度、脑含水量、神经元退化、神经元凋亡。检测氧化应激标记物和炎症因子的表达。采用免疫组化和蛋白质免疫印迹(western blotting)分析SDF-1/CXCR4信号通路活性。结果:与ICH组相比,ICH+舒芬太尼组可减轻神经系统损伤、脑含水量及细胞凋亡(P<0.05),抑制ICH后脑组织抑制丙二醛和促炎因子(IL-1β和TNF-α)的水平,提高总超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和抗炎因子(IL-10)的水平(P<0.05)。舒芬太尼可抑制ICH后大鼠脑组织中SDF-1/CXCR4信号通路活性。结论:舒芬太尼可能通过抑制SDF-1/CXCR4信号通路活性促进ICH大鼠的神经功能恢复。

     

    Abstract: Objective: To investigate the effect of sufentanil on neurological recovery in rats with intracerebral hemorrhage(ICH) by regulating the SDF-1/CXCR4 signaling pathway and the underlying mechanism. Methods: The brain injury model of ICH induced by collagenase was established, and the rats were divided into 4 groups:control group (sham operation treatment, sham group), ICH model induction group(ICH group), ICH + DMSO group(rats were treated with DMSO after ICH model), and ICH+sufentanil group (rats were treated with sufentanil 50 mg/kg.d-1 after ICH model). Biochemical analysis was used to evaluate nerve severity, brain water content, neuronal degeneration, and neuronal apoptosis. The expression of oxidative stress markers and inflammatory factors were detected. The activity of SDF-1/CXCR4 signaling pathway was analyzed by immunohistochemistry and western blotting. Results: Compared with the ICH group, the ICH + sufentanil group could reduce nervous system damage, brain water content and apoptosis(P<0.05), inhibit the levels of malondialdehyde and pro-inflammatory factors(IL-1β and TNF-α) in the brain tissue after ICH, and increase the levels of total superoxide dismutase(SOD), glutathione peroxidase (GSH-Px) and anti-inflammatory factors(IL-10)(P<0.05). Sufentanil could inhibit the activity of SDF-1/CXCR4 signaling pathway in the rat brain tissue after ICH. Conclusion: Sufentanil may promote the recovery of neurological function in ICH rats by inhibiting the activity of SDF-1/CXCR4 signaling pathway.

     

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