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目的观察羟甲基戊二酰辅酶A(HMG-CoA)还原酶抑制剂阿托伐他汀对大鼠哮喘模型气道重建的影响。方法将80只SD雄性大鼠随机分为4组:空白对照组、哮喘组、地塞米松组、阿托伐他汀组。以10g/L卵白蛋白(OVA)腹腔注射致敏并长期吸入,激发制备慢性哮喘模型。用免疫组织化学方法检测各组大鼠肺组织中过氧化物酶体增殖因子活化受体γ(PPAR-γ)、NF-κβ、Ⅲ型胶原的表达,同时图像分析方法测量气道壁内周长、平滑肌面积。结果 1.阿托伐他汀组的大鼠肺内嗜酸性粒细胞、淋巴细胞降低,肺组织中PPAR-γ表达增加,NF-κβ阳性细胞数降低与对照组比较差异具有统计学意义(P<0.05),与地塞米松组相比差异无统计学意义(P>0.05);PPAR-γ在肺内表达量与NF-κβ的活化细胞数呈负相关(rs=-0.530,P<0.05)。2.阿托伐他汀组支气管管壁面积(WAm)/Pi、平滑肌面积/Pi、N/Pi、Ⅲ型胶原的表达降低,与对照组比较差异具有统计学意义(P<0.05);与地塞米松组相比差异无统计学意义(P>0.05)。结论阿托伐他汀具有促进哮喘大鼠PPAR-γ的产生,抑制NF-κβ的活化,可延缓哮喘气道重建的进程,其抑制增生的作用与地塞米松类似。
Objective To observe the effects of HMG-CoA reductase inhibitor atorvastatin on airway remodeling in a rat model of asthma. Methods Eighty SD male rats were randomly divided into 4 groups: control group, asthma group, dexamethasone group and atorvastatin group. To 10g / L ovalbumin (OVA) intraperitoneal injection sensitized and long-term inhalation, stimulate the preparation of chronic asthma model. The expression of peroxisome proliferator-activated receptor γ (PPAR-γ), NF-κβ and type Ⅲ collagen in the lung tissue of rats in each group were detected by immunohistochemical method. At the same time, Long, smooth muscle area. Results 1. Atorvastatin group decreased lung eosinophils and lymphocytes, PPAR-γ expression in lung tissue increased, NF-κβ positive cells decreased compared with the control group was statistically significant (P < 0.05). There was no significant difference between dexamethasone group and dexamethasone group (P> 0.05). The expression of PPAR-γ in the lung was negatively correlated with the number of activated NF-κβ (rs = -0.530, P <0.05) . Compared with control group, the difference of bronchial wall area (Pi), Pi, smooth muscle area / Pi, N / Pi and type Ⅲ collagen in Atorvastatin group was statistically significant (P <0.05) There was no significant difference between the two groups (P> 0.05). Conclusions Atorvastatin can promote the production of PPAR-γ, inhibit the activation of NF-κβ in asthmatic rats and delay the process of airway remodeling in asthmatic rats. Its inhibitory effect on proliferation is similar to that of dexamethasone.