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Int J Med Sci. 2015 Aug 28;12(9):708-18. doi: 10.7150/ijms.12032. eCollection 2015.

Secondhand Smoke Exposure Reduced the Compensatory Effects of IGF-I Growth Signaling in the Aging Rat Hearts.

Author information

1
1. Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
2
2. School of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan.
3
3. Department of Biological Science and Technology, China Medical University, Taichung.
4
4. Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan.
5
5. Division of Cardiology, China Medical University Hospital, Taichung, Taiwan.
6
6. Department of pathology, Changhua Christian Hospital, Changhua ; 7. Department of Medical Technology, Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli, Taiwan.
7
8. Orthopaedic Department, Armed Forces General Hospital, Taichung, Taiwan.
8
9. Department of Biotechnology, Bharathiar University, Coimbatore-641 046, India.
9
10. Department of Nursing, Mei Ho University, 23 Pingguang Road, Pingtung 91202, Taiwan.
10
1. Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan ; 11. School of Chinese Medicine, China Medical University, 91 Hsueh-Shih Road, Taichung 40402, Taiwan ; 12. Department of Health and Nutrition Biotechnology, Asia University, 500 Lioufeng Road, Taichung 41354, Taiwan.

Abstract

BACKGROUND:

Secondhand smoke (SHS) exposure is associated with increased risk of cardiovascular disease. Aging is a physiological process that involves progressive impairment of normal heart functions due to increased vulnerability to damage. This study examines secondhand smoke exposure in aging rats to determine the age-related death-survival balance.

METHODS:

Rats were placed into a SHS exposure chamber and exposed to smog. Old age male Sprague-Dawley rats were exposed to 10 cigarettes for 30 min, day and night, continuing for one week. After 4 weeks the rats underwent morphological and functional studies. Left ventricular sections were stained with hematoxylin-eosin for histopathological examination. TUNEL detected apoptosis cells and protein expression related death and survival pathway were analyzed using western blot.

RESULTS:

Death receptor-dependent apoptosis upregulation pathways and the mitochondria apoptosis proteins were apparent in young SHS exposure and old age rats. These biological markers were enhanced in aging SHS-exposed rats. The survival pathway was found to exhibit compensation only in young SHS-exposed rats, but not in the aging rats. Further decrease in the activity of this pathway was observed in aging SHS-exposed rats. TUNEL apoptotic positive cells were increased in young SHS-exposed rats, and in aging rats with or without SHS-exposure.

CONCLUSIONS:

Aging reduces IGF-I compensated signaling with accelerated cardiac apoptotic effects from second-hand smoke.

KEYWORDS:

Secondhand smoke exposure; age-related death-survival balance; aging; apoptosis.; cell cycle

PMID:
26392808
PMCID:
PMC4571548
DOI:
10.7150/ijms.12032
[Indexed for MEDLINE]
Free PMC Article

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