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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。
Objective: To investigate the mechanism of Liangqi powder on inflammation induced by endotoxin in acute lung injury in rats. METHODS: Rat models of acute lung injury were established by intravenous injection of endotoxin lipopolysaccharide (LPS). The treatment was performed with Liangyu Powder. After the end of the experiment, the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-10 (IL-10) in rat serum were measured. And lung wet/dry mass ratio. RESULTS: Compared with the control group, the TNF-α content in the LPS group began to increase 1 h after LPS injury, reached the peak at 2 h (P<0.01), and then decreased rapidly; the IL-1β content was 2 h after LPS injury. Significantly increased, peaked at 8h (P<0.05), then decreased rapidly; IL-10 content began to increase at 2h after LPS injury (P<0.05). Compared with the LPS group, the ratios of TNF-α, IL-1β, and wet/dry weight ratio of rat lung were significantly decreased in Liangliang Powder and dexamethasone groups, and IL-10 was significantly increased (P<0.05 or P<0.01). Conclusion: Liangyu Powder can reduce lung injury. Its mechanism may be to inhibit the release of inflammatory mediators by promoting the secretion of anti-inflammatory mediators, thereby regulating the balance between inflammation and anti-inflammatory responses.