左旋肉碱对大鼠缺血性脑损伤的神经保护作用

Neuroprotective effect of L-carnitine on ischemic brain injury in rats

目的观察左旋肉碱(L-carnitine,LC)对大鼠早期缺血性脑损伤和低氧低糖诱导神经细胞损伤的保护作用,并探讨其可能的作用机制。方法线栓法制备大鼠局灶性脑缺血模型。TTC染色法观察脑梗死面积的改变。采用连二亚硫酸钠(Na2S2O4)合并低糖培养基培养PC12细胞,建立体外细胞低氧低糖模型;MTT法检测细胞活力的改变;SYTOX、PI、TUNEL染色观察细胞的坏死与凋亡;检测各组细胞SOD、ATP酶活性和MDA含量。结果LC预处理组大鼠脑梗死灶面积较模型组无明显减小(P>0.05)。LC预处理可使低氧低糖诱导的细胞活力增加,坏死与凋亡减少,细胞内SOD、ATP酶活性增高,MDA含量降低(P<0.05)。结论短期急性注射LC对大鼠缺血性脑损伤保护作用不明显,对体外低氧低糖诱导的PC12细胞损伤具有明显保护作用,其机制可能与增强细胞抗氧化能力、抑制脂质过氧化反应、减少细胞凋亡与坏死有关。

Objective To observe the protective effect of L-carnitine on ischemic brain injury in rats and oxygen-glucose deprivation（OGD） induced damage in PC12 cells,and to explore its possible mechanisms.Methods The focal cerebral ischemia rat models were made by the suture method.The infarction size was assessed by TTC staining.In vitro,PC12 cells were treated with sodium hydrosulfite（Na2S2O4） in combination with glucose deprivation.Cell viability was analyzed by using MTT assay while the necrosis and apoptosis were observed with SYTOX,PI,TUNEL staining.In addition,the activities of ATPase and SOD,as well as the MDA content,were also detected.Results The infarction size in the LC group was not obviously reduced compared with that of the model group by using TTC staining（P0.05）.In vitro,when we pretreated PC12 cells with LC,the cell viability,the activities of SOD and ATPase increased,while the number of apoptotic and necrotic cells,as well as the content of MDA decreased,compared with those of the OGD group（P0.05）.Conclusion Short-term acute L-carnitine injection has no significant protective effect on ischemic brain injury in rats,but it could protect PC12 cells against oxygenglucose deprivation from damage,and it may exerte these effects through improving cell antioxidant capacity,inhibiting the lipid peroxidation,cell apoptosis and necrosis.