桔梗总皂苷对大鼠急性肺损伤保护作用及机制

Protective effects of Platycodon grandiflorum total saponins on acute lung injury in rats and relatedmechanisms

目的探讨桔梗总皂苷对大鼠急性肺损伤的保护作用及可能机制。方法60只sD大鼠随机（随机数字法）分为对照组、模型组、桔梗总皂苷低、中、高剂量组、地塞米松组，每组10只。低、中、高剂量组和地塞米松组分别腹腔注射50、100、200mg／kg桔梗总皂苷和5mg／妇地塞米松，1h后5组按10mg／kg剂量腹腔注射脂多糖造模，观察大鼠的临床症状。12h后，麻醉采血及取材，测定大鼠动脉血氧分压及二氧化碳分压、血清TNF-α和IL-10含量、肺组织湿／干质量比（W／D）、肺组织中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物（GSH-PGSH-Px）活性和丙二醛（MDA）水平、NF-κB蛋白表达等指标。结果模型组大鼠出现明显的急性肺损伤症状和肺组织病变。与模型组相比，适当剂量的桔梗总皂苷处理组急性肺损伤症状和肺组织病变明显减轻，大鼠动脉血氧分压显著升高（P〈0．05）、二氧化碳分压显著降低（P〈0．05）、血清TNF-α水平显著降低（P〈0．05）、IL-10水平显著升（P〈0．05），肺组织W／D比值显著降低（P〈0．05），SOD和GSH-Px水平显著升高（P〈0．05），MDA水平显著降低（P〈0．05），NF-κB水平显著降低（P〈0．05）。结论桔梗总皂苷对大鼠急性肺损伤具有明显的保护作用，作用机制可能与其抗体内炎症、抗脂质过氧化和下调肺组织中NF—κB蛋白表达有关。

Objective To investigate the protective effects of Platycodon grandiflomm total saponins （PGTS） on acute lung injury （ALI） in rats and the related mechanisms. Methods Total of 60 SD rats were randomly （random number） divided into control group, model group, low-, middle- and high-dose PGTS group, and dexamethasone group, 10 rats in each group. The latter 4 groups and dexamethasone group were injected with 50, 100, 200 mg/kg PGTS and 5 mg/kg dexamethasone, respectively. After 1 h, the latter 5 groups were intraperitoneally injected with mg/kg LPS to establish the ALI model. The clinical symptoms of the rats were observed. After 12 h, the arterial PaO2 and PaCO2, serum TNF-α and IL-10 level, lung wet/dry weight ratio （W/D）, lung tissue SOD, GSH-Px and MDA level and NF-κB protein expression were determined. Results Rats in model group manifested noticeable symptoms of acute lung injury （ALI） and lung tissue lesions. In trexttment group with appropriate PGTS dose, ALI symptoms and lung lesions were significantly alleviated, arterial PaO2 was markedly increased （P 〈0. 05）, PaCO2 was decreased obviously （P 〈0. 05）, serum TNF-α level was prominently decreased （P 〈 0. 05 ）, IL-10 level was strikingly decreased （P 〈 0. 05 ）, lung W/D ratio was significantly decreased （P 〈 0. 05）, lung tissue SOD and GSH-Px level were distinctly increased （ P 〈 0. 05）, MDA was clearly decreased （P 〈 0. 05）, and NF-κB protein expression was plainly decreased （ P 〈 0. 05 ）, compared with model group. Conclusions PGTS has undoubted protective effects on acute lung injury induced by LPS in rats. The mechanism may be associated with its role of anti-inflammation, anti-lipid peroxidation and down regulation of NF-κB protein level in lung tissue.