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

Q3 Medicine Endocrine and Metabolic Science Pub Date : 2021-09-30 DOI:10.1016/j.endmts.2021.100097

Ayodeji Folorunsho Ajayi , Olubodun Micheal Lateef , Oluwadunsi Iyanuoluwa Adebayo , Emmanuel Tayo Adebayo

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引用次数: 2

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.

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Hsps70和90通过产生一氧化氮和VEGF抑制细胞凋亡来保护甲状腺功能亢进大鼠的心脏

背景。甲状腺状态改变时，心脏的收缩和代谢需求发生变化。这些变化可能与血管内皮生长因子(VEGF)的细胞信号传导和热休克蛋白(Hsp)表达的改变有关。本研究观察甲状腺功能障碍对甲状腺功能障碍大鼠心脏组织中VEGF、hsp70、hsp90浓度的影响。Wistar大鼠随机分为对照组、甲亢组(左旋甲状腺素组)和甲亢组(卡比马唑组)。采用标准方法检测甲状腺功能、体重变化、血清肌酐激酶(CK-MB)、心肌肌钙蛋白I (cTnI)、肌钙蛋白T (cTnT)、NO、VEGF、Hsp70、hsp90。甲状腺功能亢进组NO、VEGF、Hsp70、hsp90水平较对照组显著升高(p < 0.05)，甲状腺功能低下组表达较对照组降低。卡咪唑治疗导致甲状腺功能减退组脂质过氧化和CK-MB水平显著升高，超氧化物歧化酶(SOD)活性显著降低。在甲状腺功能亢进大鼠心脏组织中，Hsp70和90的表达增加，通过促进一氧化氮的产生和VEGF抑制细胞凋亡，在保护心脏免受氧化损伤和心血管紊乱中发挥重要作用。

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