Gu Ming-Xiao, Liu Xuan-Cheng, Jiang Lu
Department of Neonatology, Qingdao Women and Children's Hospital，Qingdao Shandong 266034, China.
Zhongguo Dang Dai Er Ke Za Zhi. 2013 Jul;15(7):583-7.
To investigate the effects of peroxisome proliferator-activated receptor-gamma (PPARγ) agonist rosiglitazone on the expression of cyclin D1 in lung tissue, and the proliferation of airway smooth muscle cells (ASMCs) in mice with bronchial asthma.
Thirty clean BALB/c mice were randomly divided into control group (n = 10), asthma group (n = 10), and rosiglitazone treatment group (n = 10). A mouse model of asthma was established by ovalbumin (OVA) sensitization and challenge. The treatment group received rosiglitazone (5 mg/kg) by gavage 1 hour before each challenge and the control group received saline instead of OVA sensitization and challenge. Leukocytes and eosinophils in bronchoalveolar lavage fluid (BALF) were counted under a microscope. Airway structural changes were observed by hematoxylin-eosin staining. Protein and mRNA expression levels of cyclin D1 were measured by immunohistochemical staining and RT-PCR. Perimeter of the basement membrane (Pbm), total bronchial wall area (WAt), airway smooth muscle area (WAm), and number of nuclei in ASMCs (N) were determined using image analysis software, and WAt/Pbm, WAm/Pbm, and N/Pbm were calculated.
Compared with the control group, the asthma group showed significant increases in the total number of leukocytes and percentage of eosinophils in BALF, as well as in the mRNA and protein expression of cyclin D1, but changes in these indices were significantly reduced in the rosiglitazone treatment group (P < 0.05). In addition, compared with the control group, the asthma group had significantly increased WAt/Pbm, WAm/Pbm, and N/Pbm, but rosiglitazone significantly decreased these ratios (P < 0.05).
Rosiglitazone may delay the process of airway remodeling by inhibiting the proliferation of ASMCs, so it can be used for preventing and treating chronic asthma.
探讨过氧化物酶体增殖物激活受体γ（PPARγ）激动剂罗格列酮对支气管哮喘小鼠肺组织细胞周期蛋白D1表达及气道平滑肌细胞（ASMCs）增殖的影响。
将30只清洁级BALB/c小鼠随机分为对照组（n = 10）、哮喘组（n = 10）和罗格列酮治疗组（n = 10）。通过卵清蛋白（OVA）致敏和激发建立小鼠哮喘模型。治疗组在每次激发前1小时经口灌胃给予罗格列酮（5 mg/kg），对照组给予生理盐水且不进行OVA致敏和激发。在显微镜下计数支气管肺泡灌洗液（BALF）中的白细胞和嗜酸性粒细胞。采用苏木精-伊红染色观察气道结构变化。通过免疫组织化学染色和RT-PCR检测细胞周期蛋白D1的蛋白和mRNA表达水平。使用图像分析软件测定基底膜周长（Pbm）、总支气管壁面积（WAt）、气道平滑肌面积（WAm）和ASMCs中的细胞核数量（N），并计算WAt/Pbm、WAm/Pbm和N/Pbm。
与对照组相比，哮喘组BALF中白细胞总数和嗜酸性粒细胞百分比以及细胞周期蛋白D1的mRNA和蛋白表达均显著增加，但罗格列酮治疗组这些指标的变化明显降低（P < 0.05）。此外，与对照组相比，哮喘组WAt/Pbm、WAm/Pbm和N/Pbm显著增加，但罗格列酮显著降低了这些比值（P < 0.05）。
罗格列酮可能通过抑制ASMCs增殖延缓气道重塑进程，可用于防治慢性哮喘。
