Effects of Insulin-Like Growth Factor-1 on Apoptosis of Diaphgramatic Muscle Cell and Pulmonary Function in Rats with COPD_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

 SUN Lihua , OUYANG Xiaoping , GU Wei , TAN Yan , GAO Jingpeng

Department of Respiratory Medicine, Nanjing First Hospital Affiliated to Nanjing Medical University. Nanjing,Jiangsu, 210006, China Corresponding Author: SUN Li-hua, E-mail: nfhsun@ sina. com;

Corresponding author：

SUN Lihua, Email: nfhsun@sina.com

Keywords：

Chronic obstructive pulmonary disease; Insulin-like growth factor-1; Diaphragm; Apoptosis; Pulmonary function; Fas / FasL

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Objective To investigate the protective effects of recombinant human insulin-like growth factor-1 ( rhIGF-1) on apoptosis of diaphragm in rats with COPD and its impact on pulmonary function. Methods Forty-five male Wistar rats were randomly divided into three groups, ie. a normal control group, a model group, and an IGF-1 intervention group, with 15 rats in each group. The rats in the model group and IGF-1 group were exposed to 5% smoke ( 30 min perday, lasting 28 days) in a sealed box, and 200 μg lipopolysaccharide was injected intratracheally on the 1st and 14th day. The rats in the IGF-1 group were given rhIGF-1 ( 60 μg /100 g) additionally by subcutaneous injection once a day, lasting 28 days. On the 1st, 14th, 28th day, 5 rats from each group were sacrificed. The weight, rate of apoptosis, Fas gene and Fas protein expression of isolated diaphragms were detected. The pulmonary function was measured on the 28th day before sacrificed. Results The mass of diaphragms, minute ventilation ( VE) , peak expiratory flow ( PEF) , inspiratory capacity ( IC) , forced expiratory volume in 0. 3 second ( FEV0. 3) of themodel groupand IGF-1 group were all decreased compared with the control group ( P lt; 0. 05) . The mass of diaphragms, VE, IC of the IGF-1 group were higher than those of the model group ( P lt;0. 05) , and the differences of PEF and FEV0. 3 were not significant ( P gt; 0. 05) . On the 14th, 28th day, rate of apoptosis, Fas gene and protein expressions in the IGF-1 group were lower than those in the model group, and still higher than those in the control group ( P lt; 0. 05) . Conclusions Fas/FasL mediated apoptosis way is involved in the diaphragm apoptosis. rhIGF-1 may reduce the apoptosis of the diaphragmand improve the VE and IC of rats with COPD by intervening Fas/FasL pathway.

Citation： SUN Lihua,OUYANG Xiaoping,GU Wei,TAN Yan,GAO Jingpeng. Effects of Insulin-Like Growth Factor-1 on Apoptosis of Diaphgramatic Muscle Cell and Pulmonary Function in Rats with COPD. Chinese Journal of Respiratory and Critical Care Medicine, 2009, 09(5): 441-445. doi: Copy

1.	Gosker HR, Wouters EF, van der Vusse GJ, et al. Skeletal muscle dysfunction in chronic obstructive pulmonary disease and chronic heart failure: underlying mechanisms and therapy perspectives. Am J Clin Nutr, 2000, 71: 1033-1047.
2.	Ottenheijm CA, Heunks LM, Sieck GC, et al. Diaphragm dysfunction in chronic obstructive pulmonary disease. Am J Respir Crit Care Med, 2005, 172: 200-205.
3.	Degens H, Swisher AK, Heijdra YF, et al. Apoptosis and Id2 expression in diaphragm and soleus muscle from the emphysematous hamster. Am J Physiol Regul Integr Comp Physiol, 2007, 293: 135- 144.
4.	林建海, 杨玲, 鲁慧敏. 精氨酸对慢性阻塞性肺疾病呼吸衰竭合并营养不良的作用. 中国呼吸与危重监护杂志, 2004, 3: 91-93.
5.	Pérez R, García-Fernández M, Díaz-Sánchez M, et al. Mitochondrial protection by low doses of insulin-like growth factor-Ⅰ in experimental cirrhosis. World J Gastroenterol, 2008, 14 : 2731 -2739 .
6.	宋一平, 崔德健, 茅培英, 等. 慢性阻塞性肺疾病大鼠模型的建立及药物干预的影响. 中华内科杂志, 2000, 39: 556-557.
7.	纪勇, 陈国强, 黄斌, 等. Caspase 抑制剂对大鼠心肌缺血/ 再灌注损伤Fas /FasL 表达的影响. 中国微循环, 2009, 2: 102-104.
8.	Radell PJ, Eleff SM, Nichols DG. Effects of loaded breathing and hypoxia on diaphgram metabolism as measured by ( 31 ) P-NMP spectroscopy. Appl Physiol, 2000, 88: 933-938.
9.	Barreiro E, de la Puente B, Minguella J, et al. Oxidative stress and respiratory muscle dysfunction in severe chronic obstructive pulmonary disease. Am J Respir Crit Care Med, 2005 , 171: 1116 - 1124.
10.	Fournier M, Huang ZS, Li H, et al. Insulin-like growth factor I prevents corticosteroid-induced diaphragm muscle atrophy in emphysematous hamsters. Am J Physiol Regul Integr Comp Physiol, 2003, 285: R34-R43.
11.	Diaz O, Villafranca C, Ghezzo H, et al. Role of inspiratory capacity on exercise tolerance in COPD patients with and without tidal expiratory flow limitation at rest. Eur Respir J, 2000, 16: 269-275.
12.	O′Donnell DE, Forkert L, Webb KA. Evaluation of bronchodilator responses in patients with “irreversible”emphysema. Eur Respir J, 2001, 18: 914-920.
13.	Boni E, Corda L, Franchini D, et al. Volume effect and exertional dyspnoea after bronchodilator in COPD patients with and without expiratory flow limitation at rest. Thorax, 2002, 57: 528-532.
14.	Marin JM, Carrizo SJ, Gascon M, et al. Inspiratory capacity, dynamic hyperinflation, breathlessness, and exercise performance during the 6-minute-walk test in chronic obstructive pulmonary disease. Am J Respir Crit Care Med, 2001, 163: 1395-1399.

1. Gosker HR, Wouters EF, van der Vusse GJ, et al. Skeletal muscle dysfunction in chronic obstructive pulmonary disease and chronic heart failure: underlying mechanisms and therapy perspectives. Am J Clin Nutr, 2000, 71: 1033-1047.
2. Ottenheijm CA, Heunks LM, Sieck GC, et al. Diaphragm dysfunction in chronic obstructive pulmonary disease. Am J Respir Crit Care Med, 2005, 172: 200-205.
3. Degens H, Swisher AK, Heijdra YF, et al. Apoptosis and Id2 expression in diaphragm and soleus muscle from the emphysematous hamster. Am J Physiol Regul Integr Comp Physiol, 2007, 293: 135- 144.
4. 林建海, 杨玲, 鲁慧敏. 精氨酸对慢性阻塞性肺疾病呼吸衰竭合并营养不良的作用. 中国呼吸与危重监护杂志, 2004, 3: 91-93.
5. Pérez R, García-Fernández M, Díaz-Sánchez M, et al. Mitochondrial protection by low doses of insulin-like growth factor-Ⅰ in experimental cirrhosis. World J Gastroenterol, 2008, 14 : 2731 -2739 .
6. 宋一平, 崔德健, 茅培英, 等. 慢性阻塞性肺疾病大鼠模型的建立及药物干预的影响. 中华内科杂志, 2000, 39: 556-557.
7. 纪勇, 陈国强, 黄斌, 等. Caspase 抑制剂对大鼠心肌缺血/ 再灌注损伤Fas /FasL 表达的影响. 中国微循环, 2009, 2: 102-104.
8. Radell PJ, Eleff SM, Nichols DG. Effects of loaded breathing and hypoxia on diaphgram metabolism as measured by ( 31 ) P-NMP spectroscopy. Appl Physiol, 2000, 88: 933-938.
9. Barreiro E, de la Puente B, Minguella J, et al. Oxidative stress and respiratory muscle dysfunction in severe chronic obstructive pulmonary disease. Am J Respir Crit Care Med, 2005 , 171: 1116 - 1124.
10. Fournier M, Huang ZS, Li H, et al. Insulin-like growth factor I prevents corticosteroid-induced diaphragm muscle atrophy in emphysematous hamsters. Am J Physiol Regul Integr Comp Physiol, 2003, 285: R34-R43.
11. Diaz O, Villafranca C, Ghezzo H, et al. Role of inspiratory capacity on exercise tolerance in COPD patients with and without tidal expiratory flow limitation at rest. Eur Respir J, 2000, 16: 269-275.
12. O′Donnell DE, Forkert L, Webb KA. Evaluation of bronchodilator responses in patients with “irreversible”emphysema. Eur Respir J, 2001, 18: 914-920.
13. Boni E, Corda L, Franchini D, et al. Volume effect and exertional dyspnoea after bronchodilator in COPD patients with and without expiratory flow limitation at rest. Thorax, 2002, 57: 528-532.
14. Marin JM, Carrizo SJ, Gascon M, et al. Inspiratory capacity, dynamic hyperinflation, breathlessness, and exercise performance during the 6-minute-walk test in chronic obstructive pulmonary disease. Am J Respir Crit Care Med, 2001, 163: 1395-1399.

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