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目的探讨不同剂量1,25二羟基维生素预处理对局灶性脑缺血再灌注损伤的保护作用及机制。方法将60只SD雄性大鼠随机分为假手术组、模型组和VD30.5、1.0、1.5μg/kg预处理组,比较各组神经行为评分、炎性因子及TRL2、4水平。结果与模型组相比,随着VD3剂量的增加,神经行为评分和脑梗死面积均明显减少,VD3-3组改善最为明显(P<0.05);随着剂量的增高,各实验组IL-6和TNF-α水平降低越明显,具有明显的剂量变化趋势(P<0.05);IL-10、MDA各组变化差异无统计学意义(P>0.05);VD3各组TRL2和TRL4均明显低于模型组,且随着VD3剂量增加,TRL2和TRL4降低程度明显增加(P<0.05);再灌注5d后观察各组大鼠存活情况,以VD3-3组为最高83.33%,差异具有统计学意义(P<0.05)。结论 VD3对局灶性脑缺血再灌注损伤的保护作用具有剂量依赖性,其机制可能与抑制TLR2、4信号转导通路,减少炎性因子产生有关。
Objective To investigate the protective effects and mechanisms of different doses of 1,25-dihydroxyvitamin pretreatment on focal cerebral ischemia-reperfusion injury. Methods Sixty SD male rats were randomly divided into sham operation group, model group and VD30.5, 1.0, 1.5 μg / kg pretreatment group. Neurobehavioral score, inflammatory factor and TRL2, 4 were compared between groups. Results Compared with the model group, the scores of neurobehavioral and cerebral infarction were significantly decreased with the increase of VD3 dose, and the improvement of VD3-3 group was the most obvious (P <0.05). With the increase of dose, IL-6 (P <0.05). There was no significant difference in the levels of IL-10 and MDA (P> 0.05). The levels of TRL2 and TRL4 in VD3 groups were significantly lower than Model group. With the increase of VD3 dose, the decrease of TRL2 and TRL4 significantly increased (P <0.05). After 5 days of reperfusion, the survival of rats in each group was observed, the highest was 83.33% in VD3-3 group, the difference was statistically significant (P <0.05). Conclusion VD3 has a protective effect on focal cerebral ischemia-reperfusion injury in a dose-dependent manner. Its mechanism may be related to the inhibition of TLR2 and 4 signal transduction pathway and the reduction of inflammatory factors.