The protective effects of rosiglitazone in chronic obstructive pulmonary disease rat models_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

ZHONG Liandi ¹ , ZHANG Chunlai ¹ , ZUO Wanli ¹ , ZHOU Wei ² , HUANG Shengqi ³ , ZHANG Xin ^2,4 ,  HUANG Yanming ^1,4

1. Department of Respiration Medicine, Jiangmen Central Hospital, Jiangmen, Guangdong 529030, P. R. China;
2. Department of Pathology, Jiangmen Central Hospital, Jiangmen, Guangdong 529030, P. R. China;
3. Department of Clinical Laboratory, Jiangmen Central Hospital, Jiangmen, Guangdong 529030, P. R. China;
4. Clinical Experimental Center, Jiangmen Central Hospital, Jiangmen, Guangdong 529030, P. R. China;

Corresponding?author：

HUANG Yanming, Email: huangyanming_jxy@163.com

Keywords：

Chronic obstructive pulmonary disease; Rosiglitazone; Airway inflammation

DOI：

10.7507/1671-6205.201708052

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ObjectiveTo investigate the protecting effect of rosiglitazone for lung in airway-instillation- lipopolysaccharides and smoke-induced chronic obstructive pulmonary disease (COPD) rat models.MethodsFifty male Wistar rats with the SPF standard were randomly divided into 5 groups (n=10). The rats were treated by airway-instillation-lipopolysaccharides and exposing to smoking to establish COPD rat models excepted normal group, and the treatment groups were received gavage rosiglitazone of 0.1 mg/kg, 0.15 mg/kg, and 0.2 mg/kg rosiglitazone daily for 30 days, and the normal group or model group was received gavage normal saline. All rats were sacrificed after 30 days' treatment, and the lung tissue section was stained by hematoxylin and eosin. The mean linear intercept (MLI) and mean alveolar numbers (MAN) were measured in all groups. In addition, the protein levels of p-Stat3 and p-NF-κB were detected by immunohistochemistry.ResultsCompared with normal group, the inflammation and emphysema were observed in the lung of rats in model group, and the symptoms of the group treated with rosiglitazone were lighter than normal group. The lungs of rats treated with highest dose of rosiglitazone (0.2 mg/kg) were evaluated with lowest pathology assessment score among three treatment groups, but there was no significant difference of MLI or MAN among three treatment groups. Compared with normal group, the protein levels of p-Stat3 and p-NF-κB were increased in the lung and tracheal epithelium and lymphoid tissue of rats in model group, while the protein levels of p-NF-κB were decreased in these tissues and the protein levels of p-Stat3 were decreased in the lymphoid tissue after treatment with rosiglitazone, but the protein levels of p-Stat3 were not changed in the lung and tracheal epithelium.ConclusionRosiglitazone has a protective effect on the COPD rat models by inhibiting NF-κB pathway to reduce the inflammation of the lung parenchyma.

Citation： ZHONG Liandi, ZHANG Chunlai, ZUO Wanli, ZHOU Wei, HUANG Shengqi, ZHANG Xin, HUANG Yanming. The protective effects of rosiglitazone in chronic obstructive pulmonary disease rat models. Chinese Journal of Respiratory and Critical Care Medicine, 2018, 17(3): 230-236. doi: 10.7507/1671-6205.201708052 Copy

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12.	Chung SW, Kang BY, Kim SH, et al. Oxidized low density lipoprotein inhibits interleukin-12 production in lipopolysaccharide-activated mouse macrophages via direct interactions between peroxisome proliferator-activated receptor-gamma and nuclear factor-kappa B. J Biol Chem, 2000, 275(42): 32681-32687.
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16.	Zepp J A, Zacharias W J, Frank D B, et al. Distinct Mesenchymal Lineages and Niches Promote Epithelial Self-Renewal and Myofibrogenesis in the Lung. Cell, 2017, 170(6): 1134-1148.

1. Decramer M, Janssens W, Miravitlles M. Chronic obstructive pulmonary disease. Lancet, 2012, 379(9823): 1341-1351.
2. Zaher C, Halbert R, Dubois R, et al. Smoking-related diseases: the importance of COPD. Int J Tuberc Lung Dis, 2004, 8(12): 1423-1428.
3. Belvisi M G, Hele D J. Peroxisome proliferator-activated receptors as novel targets in lung disease. Chest, 2008, 134(1): 152-157.
4. Kadmiel M, Cidlowski J A. Glucocorticoid receptor signaling in health and disease. Trends Pharmacol Sci, 2013, 34(9): 518-530.
5. 胡蓉, 嚴國鋒, 姜虹, 等. 改良吸煙復合氣道內注入 LPS 法 COPD 大鼠模型的建立. 實驗動物與比較醫學, 2009, 29(3): 153-156.
6. 夏熙鄭, 巨春蓉. Smads 蛋白和轉化生長因子 β1 在大鼠慢性阻塞性肺疾病中的表達. 中國呼吸與危重監護雜志, 2006, 5(3): 193-197+245.
7. 金志賢, 王清, 郭翔, 等. 間充質干細胞移植肺氣腫大鼠肺組織病理改變及炎性因子表達變化. 山東醫藥, 2015, 55(15): 20-22.
8. 譚焰, 季磊, 谷偉, 等. 噻托溴銨對慢性阻塞性肺疾病大鼠膈肌纖維的影響. 中國呼吸與危重監護雜志, 2014, 13(4): 344-347.
9. 張凌紅, 段雅樂, 李于博, 等. 羅格列酮在大鼠體內藥動學及組織分布研究. 華東師范大學學報(自然科學版), 2011, 2011(4): 104-114.
10. 李穆瓊, 朱星枚, 李曉曄, 等. 羅格列酮鈉片在健康人體的生物等效性研究. 藥物分析雜志, 2009, 29(12): 2014-2017.
11. 張春來, 黃炎明, 鐘蓮娣. 羅格列酮對慢性阻塞性肺疾病大鼠的抗炎作用. 廣東醫學, 2017, 38(14): 2119-2121.
12. Chung SW, Kang BY, Kim SH, et al. Oxidized low density lipoprotein inhibits interleukin-12 production in lipopolysaccharide-activated mouse macrophages via direct interactions between peroxisome proliferator-activated receptor-gamma and nuclear factor-kappa B. J Biol Chem, 2000, 275(42): 32681-32687.
13. Straus D S, Glass C K. Anti-inflammatory actions of PPAR ligands: new insights on cellular and molecular mechanisms. Trends Immunol, 2007, 28(12): 551-558.
14. Das L M, Rosenjack J, Au L, et al. Hyper-inflammation and skin destruction mediated by rosiglitazone activation of macrophages in IL-6 deficiency. J Invest Dermatol, 2015, 135(2): 389-399.
15. Lakshmi S P, Reddy A T, Zhang Y, et al. Down-regulated peroxisome proliferator-activated receptor gamma (PPARgamma) in lung epithelial cells promotes a PPARgamma agonist-reversible proinflammatory phenotype in chronic obstructive pulmonary disease (COPD). J Biol Chem, 2014, 289(10): 6383-6393.
16. Zepp J A, Zacharias W J, Frank D B, et al. Distinct Mesenchymal Lineages and Niches Promote Epithelial Self-Renewal and Myofibrogenesis in the Lung. Cell, 2017, 170(6): 1134-1148.

Chinese Journal of Respiratory and Critical Care Medicine

The protective effects of rosiglitazone in chronic obstructive pulmonary disease rat models

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