吸入高浓度氢气对大鼠创伤性脑损伤的影响

Effects of inhaling high concentration hydrogen on traumatic brain injury in rats

目的研究高浓度氢气对大鼠创伤性脑损伤的影响及其机制。方法雄性SD大鼠30只,体重220~240 g,随机分为三组,每组10只:假手术组(S组)、脑创伤组(T组)和氢气治疗组(H组)。S组暴露硬脑膜但不进行撞击,T组与H组通过液压颅脑损伤撞击建立大鼠创伤性脑损伤模型,H组于术后第1天起每天吸入1 h高浓度氢气(42%H2-21%O2-37%N2),连续7 d。术后48 h采用HE染色法观察脑组织病理改变,免疫组化法检测创伤周围皮质氧化应激相关蛋白MPO和HO-1含量,尼氏染色法观察尼氏小体来判断神经元状态,术后7 d采用Western blot法检测凋亡相关蛋白bcl-2、bax以及caspase-3含量。结果与T组比较,H组神经元损伤减轻(P<0.05),异常神经细胞数量减少(P<0.05),促凋亡蛋白bax、caspase-3及氧化应激相关蛋白MPO、HO-1含量明显降低(P<0.05),抗凋亡蛋白bcl-2含量明显升高(P<0.05)。结论高浓度氢气可减轻大鼠创伤性脑损伤,其机制可能与氢气抗凋亡以及抗氧化应激作用相关。

Objective To investigate the effect and mechanism of high concentration hydrogen on traumatic brain injury in rats.Methods Thirty male Sprague Dawley(SD)rats,weighing 220-240 g,were randomly divided into sham operation group(group S),traumatic brain injury group(group T)and high concentration hydrogen gas treatment group(group H),10 rats in each group.Rats in group S were exposed dura mater but not impacted.Rats in group T and group H were induced by fluid percussion to establish traumatic brain injury model.Rats in group H inhaled high concentration hydrogen(42%H2-21%O2-37%N2)for 1 h per day continuously for 7 d from the first day of the operation.The pathological changes of brain tissue were observed within 48 h.The expressions of oxidative stress-related proteins MPO and HO-1 were detected by immunohistochemistry.Neuron status was determined by observing Nissl bodies by Nissl staining within 7 d.The expressions of apoptosis-related proteins bcl-2,bax and caspase-3 were detected by Western blot.Results Compared with group T,the neuronal damage in group H was alleviated(P<0.05),the number of abnormal nerve cells was decreased(P<0.05),and the expressions of the proapoptotic proteins bax,caspase-3 and oxidative stress related proteins MPO and HO-1 were significantly decreased(P<0.05).Compared with group T,the expression of protein bcl-2 was significantly increased in group H(P<0.05).Conclusion High concentration of hydrogen gas can alleviate traumatic brain injury in rats,and the mechanism may be related to the anti-apoptosis and anti-oxidative stress effects of hydrogen.