Treadmill exercise training prevented cardiac inflammation and fibrosis in hypertensive ovariectomized rats, possibly by decreasing angiotensin II type I receptors.
Does treadmill exercise training attenuate cardiac inflammation and fibrosis in hypertensive ovariectomized rats?
Exercise training attenuates cardiac inflammation and fibrosis in a rat model of hypertension and ovariectomy, likely by downregulating the angiotensin II type I receptor.
This study investigated the effects of exercise training on cardiac inflammatory and cardiac fibrotic pathways in female spontaneously hypertensive rats (SHR), which were divided into a sham-operated sedentary hypertensive group (SHR-S), a sedentary hypertensive ovariectomized group (SHR-O), or a hypertensive ovariectomized group with treadmill exercise training (SHR-OT; 60 min/day, 5 days/wk) for 8 wk. Normotensive female Wistar-Kyoto rats (WKY) served as controls. SOD and catalase (CAT) activities were significantly increased in the SHR-OT group, when compared with the SHR-S or SHR-O groups. The protein levels of estrogen receptor (ER)-α and ER-β became decreased in the SHR-O group, when compared with the WKY or SHR-S groups, but were not changed in the SHR-OT group. The protein level of the angiotensin II type I receptor (AT 1 R) was increased in the SHR-S group but did not further change in the SHR-O group, whereas it was decreased in the SHR-OT group. The inflammatory-related protein levels of TNF-α, p-NF-κB, cyclooxygenase 2 (COX-2), inducible nitric oxide synthase (iNOS), and IL-6, as well as the fibrotic-related protein levels of transforming growth factor-β (TGF-β), p-Smad2/3, connective tissue growth factor (CTGF), tissue-type plasminogen activator (tPA), matrix metalloproteinase (MMP)-9, and collagen I were increased in the SHR-S group and increased further in the SHR-O group, whereas they were decreased in the SHR-OT group. The coexistence of hypertension and ovariectomy additively increased cardiac inflammatory and fibrotic pathways partially through hypertension-enhanced AT 1 R and ovariectomy-depressed estrogen receptors. Exercise training appeared to suppress hypertensive ovariectomized heart-induced inflammatory and fibrotic pathways possibly through decreasing AT 1 R but not through estrogen receptors. NEW & NOTEWORTHY The coexistence of hypertension and ovariectomy appeared to increase cardiac inflammatory and fibrotic pathways likely through hypertension-enhanced angiotensin II type I receptor and ovariectomy-depressed estrogen receptors. Exercise training on a treadmill could prevent hypertensive ovariectomized heart-induced cardiac inflammation and fibrosis via an inflammatory pathway TNF-α, p-IKK-α/β, p-NF-κB, cyclooxygenase 2 (COX-2), iNOS, and IL-6 and fibrotic pathway transforming growth factor-β (TGF-β), p-Smad2/3, connective tissue growth factor (CTGF), tissue-type plasminogen activator (tPA), matrix metalloproteinase (MMP)-9, and collagen I possibly through decreasing angiotensin II type I receptor but not through estrogen receptors.
Lin et al. (Thu,) conducted a other in Hypertension and ovariectomy (animal model). Treadmill exercise training vs. Sedentary hypertensive ovariectomized rats (SHR-O) and sham-operated sedentary hypertensive rats (SHR-S) was evaluated on Cardiac inflammatory and fibrotic pathways. Treadmill exercise training prevented cardiac inflammation and fibrosis in hypertensive ovariectomized rats, possibly by decreasing angiotensin II type I receptors.