This study was to investigate the effects of exercise training on antiapoptotic pathways and mitochondrial biogenesis in ovariectomized hypertensive rats. Histopathological analysis. TUNEL assay, and Western blotting were performed on the excised hearts from female spontaneously hypertensive rats (SHR). which were divided into a sham-operated sedentary hypertensive (SHR-S), a sedentary hypertensive ovariectomized (SHR-O), and hypertensive ovariectomized rats that underwent treadmill exercise training (SHR-OT; 60 min/day, 5 days/wk) for 8 wk, along with normotensive Wistar Kyoto rats (WKY). When compared with the WKY group, the SHR-S group exhibited decreased protein levels of peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha) and mitochondrial OPA-1 (mitochondrial biogenesis) and decreased further in the SHR-O group. The protein levels of p-PI3K, p-Akt, Bcl-2, Bcl-xL (prosurvival pathways). and the protein levels of PGC-1 alpha and mitochondrial OPA1 (mitochondrial biogenesis) were increased in the SIIR-OT group, but estrogen receptor (ER)alpha and ER beta were not changed when compared with the SHR-O group. The protein levels of t-Bid, Bad. Bax, cytosolic cytochrome c. activated caspase 9, and activated caspase 3 (mitochondria-dependent apoptotic pathways), as well as Fas ligand, TNF-alpha, Fas receptors, Fas-associated death domain, activated caspase 8 (Fas receptor-dependent apoptotic pathways) were decreased in the SHR-OT group, when compared with the SHR-O group. Exercise training protection on the coexistence of hypertension and ovariectomy-induced cardiac mitochondria-dependent and Fas receptor-dependent apoptotic pathways by enhancing the Bcl2-related and mitochondrial biogenetic prosurvival pathways might provide a new therapeutic effect on cardiac protection in oophorectomized early postmenopausal hypertensive women.
NEW & NOTEWORTHY Widely dispersed cardiac apoptosis was found in the coexistence of hypertension and ovariectomy. Exercise training on a treadmill could prevent ovariectomized hypertension-induced widely dispersed cardiac apoptosis via mitochondria-dependent apoptotic pathway (t-Bid, Bad, Bax, cytosolic cytochrome c, activated caspase 9. and activated caspase 3) and Fas receptor-dependent apoptotic pathway (Fas ligand, tumor necrosis factor-alpha, Fas receptors, Fas-associated death domain, activated caspase 8. and activated caspase 3) through enhancing the Bcl2-related (p-PI3K, p-Akt, Bcl-2, Bcl-xL) and mitochondrial biogenetic (PGC-1 alpha and mitochondrial optic atrophy 1) prosurvival pathways.
[1]Weifang Med Univ, Sch Rehabil Med, Weifang, Shandong, Peoples R China.
[2]Asia Univ, Dept Phys Therapy, Taichung, Taiwan.
[3]China Med Univ, Grad Inst Clin Med Sci, Taichun, Taiwan.
[4]First Rehabil Hosp Shanghai, Shanghai, Peoples R China.
[5]Shandong Univ Tradit Chinese Med, Coll Rehabil, Jinan, Shandong, Peoples R China.
[6]Shanghai Univ Tradit Chinese Med, Peoples Hosp 7, Dept Rehabil, Shanghai, Peoples R China.
[7]Shanghai Univ Tradit Chinese Med, Sch Rehabil Sci, Shanghai, Peoples R China.
[8]China Med Univ, Grad Inst Biomed Sci, Taichung, Taiwan.
[9]China Med Univ Hosp, Translat Med Res Ctr, Taichung, Taiwan.
[10]China Med Univ, Dept Sports Med, Taichung, Taiwan.
[11]Chung Shan Med Univ, Chung Shan Med Univ Hosp, Dept Phys Med & Rehabil, Ctr Sleep Med, Taichung, Taiwan.
[12]Univ Taipei, Dept Sports Sci, Taipei, Taiwan.
[13]China Med Univ, Grad Inst Rehabil Sci, Dept Phys Therapy, 91 Hsueh Shih Rd, Taichung 40202, Taiwan.
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