中文摘要：

目的：探讨凉膈散对内毒素致大鼠急性肺损伤炎症调控机制。方法：静脉注射内毒素脂多糖（LPS）制作大鼠急性肺损伤模型。用凉膈散进行治疗,实验结束后测定大鼠血清中的肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）、白细胞介素-10（IL-10）的含量以及肺湿/干质量比值。结果：与对照组比较,LPS组大鼠TNF-α含量在LPS致伤后1h开始升高,至2h达到最高峰（P〈0.01）,随后迅速下降;IL-1β含量在LPS致伤后2h显著升高,至8h达到峰值（P〈0.05）,随后迅速下降;IL-10含量在LPS致伤后2h开始升高（P〈0.05）。凉膈散各剂量组及地塞米松组与LPS组比较,TNF-α、IL-1β、大鼠肺湿/干质量比值显著下降,IL-10明显上升（P〈0.05或P〈0.01）。结论：凉膈散能够减轻肺损伤,其作用机制可能是通过促进抗炎介质的分泌来抑制炎症介质的释放,从而调节炎症和抗炎反应之间的平衡。

英文摘要：

Objective： To search theeffects and possible mechanisms of Lianggesan on the acute lung injury（ALl） rat induced by endotoxin. Methods： Endotoxemia was induced by intravenous lipopolysaccharide （LPS,5 mg/kg）, then treated with Lianggesan. The levels of TNF-α, IL-1β and IL-10 in serum and wet-to-dry weight ratio of lung were detected. Results： In LPS group the levels of TNF-α began to increase at 1h, which reached the peaks at 2h（P 〈 0.01）, then declined significantly; IL-1β expression tended to elevate at 2h, peaked at 8h（P 〈 0.05）, then declined dramatically; IL-10 expression significantly enhanced at 2h（P 〈 0.05）. But the level of TNF-α ,IL- 1β and wet-to-dry weight ratio were significantly decreased and level of 1L- 10 was increased in DEX and three doses of Lianggesan groups compared with the LPS group（P 〈 0.05 or P 〈 0.01）. Conclusion： The results suggested that Lianggesan played a protective role in the endotoxin-induced ALl. The mechanisms of actions may be attributed to its anti-inflammatory activity that inhibits the release of pro-inflammatory cytokines, rectification imbalance between inflammatory and anti-inflammatory.