Effects of hydrogen gas inhalation on cerebral oxidative stress and inflammation after intestinal ischemia/reperfusion in rats / 中华器官移植杂志

ABSTRACT

Objective To investigate the effects of hydrogen gas inhalation on cerebral oxidative stress and inflammation after intestinal ischemia/reperfusion (I/R) in rats and to understand the mechanism of(I/R neuroprotection.Method Forty-eight healthy male SD rats weighing 285-350 g were randomly allocated to one of 3 groups (n =16 each group):sham operation group (Sham),intestinal I/R group (I/R) and intestinal IR plus hydrogen gas inhalation group (IR + H2).The I/R model was produced by occlusion of superior mesenteric artery (SMA) for 90 min followed by reperfusion.Inhalation of 2％ hydrogen gas was performed immediately after I/R for 3 h.All animals were sacrificed at 24 h after reperfusion in each group.Brain tissues of 8 animals in each group were harvested for detection of microglia by immunohistochemistry.The remaining 8 rats in each group were used for the following indicators analysis.The protein level of ionized calcium-binding adaptor molecular 1 (Iba-1,a marker of microglia) in the cortex was detected by Western blotting.The concentrations of ROS,MDA,IL-1β,IL-6,TNF-α,T-NOS,iNOS and NO in the cortex were measured.The MPO content and SOD activity were also measured.Result The Iba-1 staining was light in Sham group.However,the expression of Iba-1 was increased in I/R group,and H2 inhibited the expression of Iba-l.As compared with Sham group,the Iba-1 protein expression and the number of Iba-1 positive cells were increased significantly in I/R and I/R+ H2groups (P＜0.01 or 0.05).As compared with Sham group,ROS,MDA,IL-1β,IL-6,TNF-α,T-NOS,iNOS and NO levels,and MPO activity were also increased in I/R and I/R + H2groups (P＜0.01 or 0.05).As compared with I/R group,the above indicators in I/R + H2 group were markedly improved (P＜0.05 or 0.01).Conclusion The inhalation H2 could inhibit intestinal I/R-induced activation of microglia and reduce cerebral oxidative stress and inflarnmatory response in rats.