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川芎的生物活性成分(川芎嗪)已广泛应用于治疗心脑血管疾病。基于谷氨酸诱导PC12细胞损伤建立脑缺血再灌注损伤的细胞模型,探讨超声增强川芎嗪对谷氨酸损伤PC12细胞的保护作用机制。研究结果表明,超声能进一步加强川芎嗪对细胞的保护,其主要作用机制为:(1)抑制氧化应激和细胞凋亡相关的Bcl-2蛋白和Bax蛋白的变化从而达到抗凋亡的效果;(2)降低炎症因子(TNF-α和IL-8)的表达,减轻炎症反应损伤;(3)适当的声压可以增强川芎嗪对谷氨酸损伤PC12细胞的保护作用,但过高的声压会引起细胞损伤,导致细胞凋亡。本文的工作表明超声能够增强川芎嗪对脑缺血再灌注损伤的保护作用,为临床脑缺血再灌注损伤的治疗提供了新治疗策略。
Chuanxiong’s bioactive component (tetramethylpyrazine) has been widely used in the treatment of cardiovascular and cerebrovascular diseases. To establish a cell model of cerebral ischemia-reperfusion injury induced by glutamate-induced PC12 cells and to explore the mechanism of ultrasound-enhanced protection of tetramethylpyrazine against glutamate-induced PC12 cells. The results show that ultrasound can further strengthen the tetramethylpyrazine on cell protection, its main mechanism is: (1) inhibition of oxidative stress and apoptosis-related changes in Bcl-2 protein and Bax protein to achieve the anti-apoptotic effect ; (2) reduce the expression of inflammatory cytokines (TNF-α and IL-8), reduce the inflammatory response damage; (3) appropriate sound pressure can enhance tetramethylpyrazine on glutamate injury PC12 cells, but excessive Sound pressure can cause cell damage, leading to apoptosis. This work shows that ultrasound can enhance the protective effect of ligustrazine on cerebral ischemia-reperfusion injury and provide a new therapeutic strategy for the treatment of clinical cerebral ischemia-reperfusion injury.