Hsps70 and 90 protect the heart of hyperthyroid rats via nitric oxide production and VEGF inhibition of apoptosis

Abstract

Background: . Changes occur in the heart's contractile and metabolic demands during altered thyroid states. The changes may be associated with alterations in the cellular signaling of vascular endothelial growth factors (VEGF) and expressions of heat shock proteins (Hsp). Aim: . This study examined the effects of thyroid dysfunction on VEGF, hsp70, and hsp 90 concentrations in the heart tissues of dysthyroid rats. Methods: . Wistar rats were allocated into control, hypothyroid (Carbimazole-treated), and hyperthyroid (Levothyroxine-treated) groups randomly (n=7). Thyroid function test, body weight changes, serum creatinine kinase (CK-MB), cardiac troponin I (cTnI) and troponin T (cTnT), NO, VEGF, Hsp70, and Hsp 90 were determined using standard methods. Results: . There was a significant increase (P<0.05) in NO, VEGF, Hsp70, and Hsp 90 levels in the hyperthyroid group and reduced expression in the hypothyroid group compared to the control. Carbimazole treatment led to a significant increase in lipid peroxidation and CK-MB level, with a substantial decrease in the superoxide dismutase (SOD) activity in the hypothyroid group. Conclusion: . Increased expression of Hsp70 and 90 in hyperthyroid rats' heart tissue play essential roles in protecting the heart from oxidative damage and cardiovascular derangements via enhancement of nitric oxide production and apoptosis inhibition by VEGF.

Keywords

• Thyroid hormones
• Oxidative stress
• Heat shock proteins
• Cardiac dysfunction
• Cardioprotection