Treadmill Exercise Preconditioning Attenuates Lung Damage Caused by Systemic Endotoxemia in Type 1 Diabetic Rats

Author:

Hung Ching-Hsia1ORCID,Tzeng Jann-Inn23,Chang Che-Ning1,Chen Yu-Wen4,Cho Chia-Ying1,Wang Jhi-Joung5

Affiliation:

1. Department of Physical Therapy, National Cheng Kung University, Tainan 701, Taiwan

2. Department of Food Sciences and Technology, Chia Nan University of Pharmacy and Sciences, Jen-Te, Tainan 717, Taiwan

3. Department of Anesthesiology, Chi-Mei Medical Center, Yong Kang, Tainan 710, Taiwan

4. Department of Physical Therapy, China Medical University, Taichung 404, Taiwan

5. Department of Medical Research, Chi-Mei Medical Centre, Tainan 710, Taiwan

Abstract

Endotoxemia induces a series of inflammatory responses that may result in lung injury. However, heat shock protein72 (HSP72) has the potential to protect the lungs from damage. The objective of this study was to determine whether prior exercise conditioning could increase the expression of HSP72 in the lungs and attenuate lung damage in diabetic rats receiving lipopolysaccharide (LPS). Streptozotocin was used to induce diabetes in adult male Wistar rats. Rats were randomly assigned to sedentary or exercise groups. Rats in the exercise condition ran on a treadmill 5 days/week, 30–60 min/day, with an intensity of 1.0 mile/hour over a 3-week period. Rats received an intravenous infusion of LPS after 24 hrs from the last training session. Elevated lavage tumor necrosis factor-alpha (TNF-α) level in response to LPS was more marked in diabetic rats. HSP72 expression in lungs was significantly increased after exercise conditioning, but less pronounced in diabetic rats. After administration of LPS, exercised rats displayed higher survival rate as well as decreased lavage TNF-αlevel and lung edema in comparison to sedentary rats. Our findings suggest that exercise conditioning could attenuate the occurrence of inflammatory responses and lung damage, thereby reducing mortality rate in diabetic rats during endotoxemia.

Funder

National Science Council

Publisher

Hindawi Limited

Subject

Endocrinology,Endocrinology, Diabetes and Metabolism

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