高压氧预处理对CIRI大鼠神经功能的影响及机制

Effect and Mechanism of Hyperbaric Oxygen Preconditioning on Neurological Function in CIRI Rats

为了探讨脑缺血再灌注损伤（cerebral ischemia reperfusion injury,CIRI）大鼠经高压氧预处理对神经功能的影响及其作用机制,本研究选取了成年雄性SPF级SD大鼠48只,采用随机数字表法分为假手术组、模型组、干预组（高压氧预处理）各16只;对比各组大鼠的神经功能评分、脑梗死体积,采用免疫组化染色检测各组大鼠缺血侧脑组织中Beclin-1、LC3-Ⅱ、BCL-2蛋白阳性表达率,测定各组大鼠缺血侧脑组织中超氧化物歧化酶（SOD）、丙二醛（MDA）及血清中S100β蛋白、白细胞介素-1β（IL-1β）、肿瘤坏死因子-α（TNF-α）的水平。本研究发现,预处理组大鼠在造模后2 h、6 h、12 h及24 h的脑梗死体积所占百分比及神经功能评分显著的小于模型组（p〈0.05）;预处理组、模型组大鼠在造模后24 h的缺血侧脑组织中Beclin-1、LC3-Ⅱ、BCL-2蛋白表达细胞所占比例、血清中S100β蛋白、IL-1β、TNF-α水平显著的高于假手术组（p〈0.05）;预处理组大鼠在造模后24 h的缺血侧脑组织中Beclin-1、LC3-Ⅱ、BCL-2蛋白表达细胞所占比例、血清中S100β蛋白、IL-1β、TNF-α水平显著的低于模型组（p〈0.05）;预处理组、模型组大鼠在造模后24 h的缺血侧脑组织中MDA含量显著的高于假手术组（p〈0.05）,SOD含量显著的低于假手术组（p〈0.05）;预处理组大鼠在造模后24 h的缺血侧脑组织中MDA含量显著的低于模型组（p〈0.05）,SOD含量显著的高于模型组（p〈0.05）。本研究的研究表明,CIRI大鼠经高压氧预处理能显著降低凋亡相关蛋白的表达,减轻氧化损伤,减轻缺血再灌注对大鼠神经功能的损伤。

In order to investigate the effect of hyperbaric oxygen preconditioning on neurological function in rats with cerebral ischemiareperfusion injury（CIRI） and its mechanism, we selected 48 adult male SPF SD rats, which were randomly divided into sham operation group, model group, intervention group（HBO） with 16 rats in each group. The study compared the neural function score and the cerebral infarction volume in rats, used immunohistochemical staining to detect the positive expression rate of Beclin-1, LC3-Ⅱ, and BCL-2 protein in the ischemic brain tissues of rats in each group, and measured the levels of superoxide dismutase hemorrhage rats（SOD）, malondialdehyde（MDA） and serum S100 protein, interleukin-1 beta（IL-1 beta）, and tumor necrosis factor alpha（TNF-alpha） in brain issues of each group. We found that the percentage of cerebral infarction volume, and nerve function scores in preconditioning group at 2 h, 6 h, 12 h and 24 h after modeling were significantly less than the model group（P〈0.05）. The proportion of expression cells of LC3-Ⅱ, Beclin-1 BCL-2 protein, serum S100 protein, IL-1 beta, and TNF-alpha in the ischemic brain tissues of the pretreatment group and model group in 24 h after modeling were significantly higher than those in the sham operation group（P〈0.05）. The proportion of expression cells of Beclin-1, LC3-Ⅱ and BCL-2 protein, serum S100 protein, IL-1 beta, and TNF-alpha of pretreatment group in 24 h after modeling were significantly lower than those in the model group（P〈0.05）. The content of MDA in the ischemic brain tissues of the rats in the pretreatment group and model group was significantly higher than that of the sham pretreatment group（P〈0.05）, while the content of SOD was significantly lower than that of sham operation group（P〈0.05）. The content of MDA in preconditioning group was significantly lower than that of model group（P〈0.05）, where as the content of SOD was significantly higher than that in the model group（P〈0.05）. Our research indicated that pretreatment with hyperbaric oxygen in CIRI rats could significantly reduce the expression of apoptosis related proteins, alleviate oxidative damage, and alleviate the injury of neural function in rats after hemorrhage and reperfusion. lower than the model group（P〈0.05）; the content of MDA was signifi-cantly higher than that of the sham pretreatment group, the rats in the model group rats in 24 h after ischemic brain tissue Group（P〈0.05）, the content of SOD was significantly lower than that of sham operation group（P〈0.05）; the content of MDA was significantly lower than that of model group rats pretreated rats in 24 h after ischemic brain tissue（P〈0.05）, the content of SOD was significantly higher than that in the model group（P〈0.05）. Our research indicated that pretreatm ent with hyperbaric oxygen in CIRI rats can significantly reduce the expression of ap optosis related proteins,alleviate oxidative damage, and alleviate the injury of neural function in rats after hemorrhage and reperfusion.