INTRODUCTION:
Ovarian hormone deprivation promotes increased expression of cardiac fibrosis in Wistar rats, resulting in functional impairments. In turn, aerobic physical exercise appears to prevent these effects. The mechanisms involved in these observations are still uncertain. Our hypothesis is that they involve alterations in the expression of mitochondrial matrix proteins. The aim of this study was to investigate, in Wistar rats subjected to ovarian hormone deprivation (ovariectomy), the relationship between increased cardiac fibrosis and mitochondrial matrix proteins, MMP-2 and calpain-1. Additionally, we investigated the role of aerobic physical exercise as a countermeasure for alterations in the expression of these proteins.
METHODS:
Female Wistar rats aged 12 weeks (N=40) were used, divided into two groups: ovariectomized (OVX group) and those subjected to sham surgery (SHAM group). Half of each group underwent aerobic physical training for 12 weeks (14th to 26th week of life). At 26 weeks of age, the rats underwent echocardiographic examination followed by euthanasia for heart removal. Subsequently, cardiac fibrosis was quantified by histological analysis, while Calpain-1 and MMP-2 expression were performed by immunofluorescence and Western Blot.
RESULTS:
Both untrained groups presented similar cardiac morphological and functional values. However, the OVX group showed increases in cardiac fibrosis, Calpain-1, and MMP-2. In turn, aerobic physical training attenuated these effects of ovariectomy.
CONCLUSION:
Ovarian hormone deprivation promotes increased cardiac fibrosis associated with higher expression of Calpain-1 and MMP-2. Aerobic physical training appears to modulate the expression of these membrane proteins, preventing the increase in cardiac fibrosis.