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目的探讨辛伐他汀对肥胖哮喘小鼠气道炎症和气道重构的影响。方法 60只C57BL/6J小鼠随机分为空白对照组、普通哮喘组、肥胖哮喘组和辛伐他汀组,每组15只。肥胖哮喘组和辛伐他汀组小鼠应用高脂饮食诱导肥胖模型,普通哮喘组、肥胖哮喘组和辛伐他汀组小鼠采用卵蛋白致敏、激发的方法建立哮喘模型。辛伐他汀组小鼠每日给予辛伐他汀40mg/kg饮水干预,余3组正常饮水。治疗4周后计数存活小鼠后麻醉,取血、收集支气管肺泡灌洗液和肺组织。计数4组支气管肺泡灌洗液中白细胞计数和各炎性细胞百分比;病理切片观察肺组织的气道重构情况;采用ELISA法检测血清瘦素水平,应用生化分析仪检测三酰甘油、总胆固醇、谷草转氨酶和谷丙转氨酶水平。结果喂养8周时,肥胖哮喘组和辛伐他汀组小鼠体质量[(25.92±0.70)、(26.02±0.66)g]明显高于对照组[(21.12±0.70)g]和普通哮喘组[(21.06±0.96)g](P<0.05);普通哮喘组、肥胖哮喘组和辛伐他汀组小鼠支气管肺泡灌洗液中白细胞计数和嗜酸粒细胞百分比明显高于对照组(P<0.05),肥胖哮喘组高于普通哮喘组和辛伐他汀组(P<0.05);普通哮喘组、肥胖哮喘组和辛伐他汀组小鼠瘦素水平[(1.60±0.15)、(2.23±0.47)、(1.52±0.23)μg/L]均明显高于对照组[(1.39±0.11)μg/L](P<0.05),辛伐他汀组低于肥胖哮喘组(P<0.05),与普通哮喘组比较差异无统计学意义(P>0.05);肥胖哮喘组小鼠总胆固醇[(6.20±0.69)mmol/L]和三酰甘油[(2.10±0.53)mmol/L]水平均明显高于对照组[(2.60±0.47)、(1.10±0.22)mmol/L]、普通哮喘组[(3.20±0.55)、(1.10±0.36)mmol/L]和辛伐他汀组[(5.20±0.42)、(1.70±0.38)mmol/L](P<0.05),辛伐他汀组高于对照组和普通哮喘组(P<0.05),对照组与普通哮喘组比较差异无统计学意义(P>0.05)。结论辛伐他汀可改善血脂代谢紊乱,降低血清瘦素水平,改善肥胖哮喘小鼠的气道炎症和重构。
Objective To investigate the effects of simvastatin on airway inflammation and airway remodeling in obese asthmatic mice. Methods Sixty C57BL / 6J mice were randomly divided into blank control group, general asthma group, obese asthma group and simvastatin group, with 15 rats in each group. The mice in obese asthma group and simvastatin group were induced by high-fat diet to induce obesity. The common asthma group, obese asthma group and simvastatin group mice were sensitized with ovalbumin and challenged to establish asthma model. Simvastatin group mice were given Simvastatin 40mg / kg drinking water intervention, the remaining three groups of normal drinking water. After 4 weeks of treatment, the surviving mice were counted for anesthesia, blood was collected, bronchoalveolar lavage fluid and lung tissue were collected. The number of white blood cells and the percentage of inflammatory cells in the bronchoalveolar lavage fluid of the four groups were counted. The airway remodeling of the lung tissue was observed by pathological sections. Serum leptin level was measured by ELISA. The triglyceride, total cholesterol , Aspartate aminotransferase, and alanine aminotransferase levels. Results Compared with the control group [(21.12 ± 0.70) g] and the normal asthma group, the body weight of obese asthma group and simvastatin group [(25.92 ± 0.70) and (26.02 ± 0.66) g] (21.06 ± 0.96) g] (P <0.05). The numbers of white blood cells and eosinophils in bronchoalveolar lavage fluid of mice in common asthma group, obese asthma group and simvastatin group were significantly higher than those in control group (P <0.05) (1.60 ± 0.15) and (2.23 ± 0.47) respectively in the asthma group, the obese asthma group and the simvastatin group (P <0.05). Compared with the normal asthma group and the simvastatin group, , (1.52 ± 0.23) μg / L] in the simvastatin group were significantly higher than those in the control group [(1.39 ± 0.11) μg / L, P <0.05) The levels of total cholesterol ([(6.20 ± 0.69) mmol / L] and triglyceride [(2.10 ± 0.53) mmol / L] in obese asthma group were significantly higher than those in control (3.20 ± 0.55) and (1.10 ± 0.36) mmol / L in normal asthma group and (5.20 ± 0.42) and (4.20 ± 0.42) mmol / L compared with those in simvastatin group (2.60 ± 0.47 and 1.10 ± 0.22 mmol / 1.70 ± 0.38) mmol / L] (P <0.05), the simvastatin group was higher than the control group and the common asthma group (P <0.05) Group and the Ordinary asthma groups was not statistically significant (P> 0.05). Conclusion Simvastatin can improve dyslipidemia, decrease serum leptin level and improve airway inflammation and remodeling in obese asthmatic mice.