黄芪注射液对脂多糖致大鼠急性肺损伤后细胞凋亡的保护作用

Protective effects of astragali injection on cell apoptosis after lipopolysacchrideinduced acute lung injury

目的:研究黄芪注射液对脂多糖所致大鼠急性肺损伤(ALI)后细胞凋亡的保护作用,探讨其可能的机制。方法:雄性Wistar大鼠200～250 g 45只,随机分成3组,NS对照组、ALI组和黄芪注射液组。后2组以颈外静脉注射脂多糖5 mg·kg^(-1)致急性肺损伤。分别观察各组呼吸频率、动脉血氧分压(PaO_2),处死后检测肺组织湿/干(W/D)比值,免疫组化法检测肺泡上皮细胞Bcl-2、Bax蛋白表达。结果:NS对照组呼吸频率为(73±s 6)次·min^(-1),PaO_2为(90．0±2．0)mmHg,W/D比值为3．287±0．024, Bax/Bcl-2为0．5±1．0;ALI组与NS对照组相比,呼吸频率增快为(112±6)次·min^(-1)(P＜0．01),PaO_2降低为(46±3)mmHg(P＜0．01),W/D比值升高为5．151±0．023(P＜0．01),Bax/Bcl-2上升为7．8±0．7(P＜0．01);黄芪注射液组与ALI组相比,呼吸频率减慢为(94±4)次·min^(-1)(P＜0．01),PaO_2上升为(84±6)mmHg(P＜0．01),W/D比值降低为4．809±0．014(P＜0．01),Bax/Bcl-2下降为0．1±0．7 (P＜0．01)。结论:黄芪注射液可能通过降低Bax/Bcl-2细胞比例抑制细胞凋亡,减轻脂多糖所致ALI。

AIM： To observe the protective effects and the mechanism of astragali injection in rats with lipopolysaccharide-induced acute lung injury （ALI）. METHODS： Forty-five rats were randomly divided into three groups： control group, ALI group, and astragali injection group. The respiratory rates and partial pressure of arterial oxygen were measured. The rats were killed and the ratios of wet/dry lung tissue were detected. The Bcl-2-positive cells and Bax-positive cells were measured using immunocytochemistry in all groups. RESULTS： In control group, the respiratory rate was （73 ± s 6） min^-1, partial pressure of arterial oxygen （PaO2） was （90.0 ± 2.0） mmHg, the ratio of wet/dry lung tissue was 3.287 ± 0.024, and Bax/Bcl-2 was 0.5 ± 1.0. Compared with control group, the respiratory rate, the ratio of W/D of lung tissue, and Bax/Bcl-2 in ALI group increased to （ 112 ± 6） min^-1, 5.151 ± 0.023, and 7.8 ± 0.7, with P 〈 0.01 respectively, and PaO2 decreased to （46 ± 3） mmHg （P 〈 0.01）. Compared with ALI group, the respiratory rate, the ratio of wet/dry lung tissue, and Bax/Bcl-2 in ALI group decreased to （94 ± 4） min^-1, 4.809 ± 0.014, and 0.1 ± 0.7, with P 〈 0.01 respectively, and PaO2 increased to （84 ± 6） mmHg （P 〈 0.01）. CONCLUSION： Astragali injection has protective effects through inhibiting the apoptosis of the pulmonary epithelium.