氢气对急性肺损伤大鼠肺组织p38 MAPK活化的影响

目的探讨氢气对脂多糖（LPS）诱导急性肺损伤大鼠的肺保护作用及其可能的分子生物学机制。方法采用腹腔注射LPS
法建立大鼠急性肺损伤模型。32只雄性SD大鼠（体质量200~250 g）随机分为4组（n=8）：生理盐水组（SA组）、氢气吸入组（SH
组）、急性肺损伤组（LA组）和急性肺损伤+氢气吸入组（LH组），氢气治疗为腹腔注射生理盐水或LPS后持续吸入混有低浓度
氢气（2%）的空气6 h，用Western blot 技术检测肺组织中p38 MAPK 的表达，用ELISA法检测肺组织及血清中TNF-α的浓度。
结果氢气吸入可以使肺组织中的活化的p38 MAPK明显降低，同时降低其下游因子TNF-α在肺组织及血清中的浓度。结论
氢气吸入可下调肺组织及血清中TNF-α的表达，此作用可能与抑制肺组织中p38 MAPK活化有关。

Effect of hydrogen inhalation on p38 MAPK activation in rats with lipopolysaccharideinduced acute lung injury

Objective To investigate the effect of hydrogen inhalation on lipopolysaccharide(LPS)-induced acute lung injury(ALI) and the underlying molecular mechanisms.Method Thirty-two male SD rats were randomly divided into 4 groups(n= 8),namely the normal saline group(SA),saline with 2% hydrogen gas inhalation group(SH group),ALI group,and ALI with hydrogen inhalation group(LH group).In the two ALI groups,ALI was induced by intraperitoneal injection of 15 mg/kg LPS.Treatments with inhalation of 2% hydrogen gas for 6 h was administered after the injection of LPS or saline.The concentrations of tumor necrosis factor-α(TNF-α) in the lung tissue and serum were examined with ELISA.The expression of p38 MAPK in the lung tissue was detected by Western blotting.Results Hydrogen inhalation decreased the expression of p-p38 MAPK in the lung tissue,and significantly reduced TNF-α content in the lung tissue and serum of rats with ALI.Conclusion Hydrogen inhalation can decrease the expression of TNF-α in the lung tissue and serum,and this effect may be related with reduced p38 MAPK expression and inhibition of p38 MAPK activation.