烟酰胺经调控p38MAPK信号通路对高血压脑出血大鼠的脑保护作用机制分析

Mechanism Analysis of the Protective Effect of Niacinamide on Hypertensive cerebral Hemorrhage in Rats by Regulating p38MAPK Signaling Pathway

目的:探讨烟酰胺经调控p38MAPK信号通路对高血压脑出血大鼠的脑保护作用机制。方法:选择48只SD大鼠,随机选择12只作为假手术组,其余36只进行高血压脑出血造模,对比4组大鼠的血肿体积、左扭转比率、神经功能变化、出血脑组织p-p38MAPK、p38MAPK蛋白表达、烟酰胺腺嘌呤二核苷酸、凋亡诱导因子含量及脑组织含水量。结果:与模型组相比,尼莫地平组、烟酰胺组的血肿体积明显缩小;与烟酰胺组相比,尼莫地平组的血肿体积明显缩小(P<0.05);与干预前相比,干预后烟酰胺组、尼莫地平组的血肿体积明显缩小,模型组的血肿体积明显增多(P<0.05)。与模型组相比,假手术组、尼莫地平组、烟酰胺组的向左扭转比率、p-p38MAPK/p38MAPK、烟酰胺腺嘌呤二核苷酸明显较高,脑组织含水量、凋亡诱导因子含量明显较低;与烟酰胺组相比,尼莫地平组、假手术组的左扭转比率、p-p38MAPK/p38MAPK、烟酰胺腺嘌呤二核苷酸明显较高,脑组织含水量、凋亡诱导因子含量明显较低;与尼莫地平组相比,假手术组的左扭转比率、p-p38MAPK/p38MAPK、烟酰胺腺嘌呤二核苷酸明显较高,脑组织含水量、凋亡诱导因子含量明显较低(P<0.05)。结论:在高血压脑出血大鼠中,p38MAPK介导的细胞凋亡途径会加剧高血压脑出血的脑损伤,烟酰胺会经过抑制p38MAPK信号通路减轻高血压脑出血后的脑损伤。

Objective:To investigate the protective effect of niacinamide on hypertensive cerebral hemorrhage in rats by regulating p38MAPK signaling pathway.Methods:48 SD rats were selected,12 were randomly selected as sham operation group,and the remaining 36 rats underwent hypertensive intracerebral hemorrhage modeling.The volume of hematoma,the ratio of left twist,the changes of nerve function,the expression of p-p38MAPK,p38MAPK protein,the contents of niacinamide adenine dinucleotide,apoptosis-inducing factors and the water content of brain tissue were compared between the four groups.Results:Compared with the model group,the hematoma volume significantly decreased in the nimodipine and nicotinamide groups;compared with the nicotinamide group(P<0.05);in the nicotinamide and nimodipine group,the hematoma volume significantly increased in the model group(P<0.05).Compared with model group,the ratio of left twisting,p-p38MAPK/p38MAPK and nicotinamide adenine dinucleotides in sham operation group,nimodipine group and niacinamide group were significantly higher,while the contents of water content and apoptosis-inducing factors in brain tssue were significantly lower.Compared with niacinamide group,the ratio of left twisting,p-p38MAPK/p38MAPK and niacinamide adenine dinucleotide in nimodipine group and sham operation group were significantly higher,and the contents of water content and apoptosis-inducing factors in brain tissue were significantly lower.Compared with Nimodipine group,the ratiooflef twist,P-P38MAPk/p38MAPK and niacinamide adenine dinucleotide in sham operation group were significantly higher,and the contents of water content and apoptosis-inducing factor in brain tissue were significantly lower(P<0.05).Conclusions:In hypertensive intracerebral hemorrhage rats,P38MAPK-mediated apoptosis pathway can aggravate the brain injury,and niacinamide can reduce the brain injury after hypertensive intracerebral hemorrhage by inhibiting p38MAPK signaling pathway.