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目的:探讨复方甘草酸苷对脂多糖(LPS)诱导大鼠肺损伤的保护作用。方法:将健康SD大鼠随机分为正常对照组、LPS组和复方甘草酸苷低、中、高剂量组,每组10只。通过腹腔注射LPS(10mg/kg)制备大鼠急性肺损伤模型,复方甘草酸苷各剂量组于制备模型6h后腹腔注射不同剂量复方甘草酸苷(4,8或16mg/kg)。各组制备模型24h后处死大鼠,观察肺组织的病理学改变,并检测血清中炎症因子(TNF-α、IL-1β及IL-10)及肺组织中凋亡相关因子(Bcl-2和Bax)的表达水平。结果:复方甘草酸苷治疗后大鼠肺组织病理损伤减轻,血清中TNF-α和IL-1β表达显著减弱(P<0.05),IL-10表达显著增强(P<0.05);肺组织中促凋亡因子Bax的表达显著减弱(P<0.05)而抗凋亡因子Bcl-2的表达显著增强(P<0.05)。结论:复方甘草酸苷对LPS诱导的大鼠急性肺损伤具有保护作用,其作用可能是通过调控炎症反应及细胞凋亡来实现的。
Objective: To investigate the protective effect of compound glycyrrhizin on lung injury induced by lipopolysaccharide (LPS) in rats. Methods: Healthy SD rats were randomly divided into normal control group, LPS group and compound glycyrrhizin low, medium and high dose group, 10 rats in each group. The acute lung injury model was induced by intraperitoneal injection of LPS (10 mg / kg). The compound glycyrrhizin groups were injected intraperitoneally with different doses of compound glycyrrhizin (4, 8 or 16 mg / kg) 6 h after the preparation of model compound. The rats in each group were sacrificed and the rats were sacrificed 24 hours later to observe the pathological changes of lung tissue. The levels of inflammatory cytokines (TNF-α, IL-1β and IL-10), and apoptosis related factors (Bcl- Bax) expression levels. Results: After treatment with compound glycyrrhizin, the pathological damage of lung tissue was relieved in rats. The expression of TNF-α and IL-1β in serum was significantly decreased (P <0.05) and the expression of IL-10 was significantly increased (P <0.05) The expression of Bax was significantly decreased (P <0.05), while the expression of anti-apoptotic factor Bcl-2 was significantly increased (P <0.05). CONCLUSION: Compound glycyrrhizin can protect LPS-induced acute lung injury in rats and its effect may be through the regulation of inflammatory reaction and apoptosis.