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左甲状腺素和维生素 E 补充治疗对甲状腺功能减退症大鼠心肌细胞氧化应激损伤及凋亡的作用。

Role of levothyroxine and vitamin E supplementation in the treatment of oxidative stress-induced injury and apoptosis of myocardial cells in hypothyroid rats.

机构信息

Department of Endorinology and Metabolism, The Second Hospital of Anhui Medical University, 678, Furong Road, Hefei, Anhui, 230601, China.

出版信息

J Endocrinol Invest. 2017 Jul;40(7):713-719. doi: 10.1007/s40618-017-0624-z. Epub 2017 Feb 17.

Abstract

OBJECTIVE

To explore the underlying mechanism and treatment of myocardial injury caused by hypothyroidism, we evaluated oxidative stress in serum and myocardial tissue of hypothyroid rats. The effect of levothyroxine (LT4) replacement therapy and vitamin E (VitE) supplementation on oxidative stress-induced injury and apoptosis of myocardial tissue is examined.

METHODS

Male Sprague-Dawley rats were divided into five groups: normal control group, propylthiouracil group (PTU group), LT4 treatment group (PTU + LT4 group), vitamin E treatment group (PTU + VitE group), and combined treatment group (PTU + LT4 + VitE group). Superoxide dismutase (SOD) activity and malondialdehyde (MDA) expression in serum and myocardium were determined. Myocardial apoptosis index (AI) in each group was determined by TUNEL assay.

RESULTS

SOD levels in serum were significantly increased in PTU + VitE and PTU + LT4 + Vit E groups, as compared to that in PTU and PTU + LT4 groups (P < 0.05). MDA levels in serum and myocardial tissue were significantly lower in PTU + LT4, PTU + VitE, and PTU + LT4 + VitE groups, as compared to that in the PTU group (P < 0.05). Myocardial apoptosis was significantly increased in PTU and PTU + VitE groups as compared to that in the normal control group (P < 0.05), while it was significantly lower in PTU + LT4 and PTU + LT4 + VitE groups, as compared to that in the PTU group (P < 0.05).

CONCLUSION

In this study, levothyroxine replacement therapy and vitamin E supplementation appeared to ameliorate myocardial apoptosis in hypothyroid rats, the mechanism of which appears to be related to improved thyroid function and reduced oxidative stress.

摘要

目的

探讨甲状腺功能减退症引起心肌损伤的潜在机制和治疗方法,我们评估了甲状腺功能减退症大鼠血清和心肌组织中的氧化应激。研究了左甲状腺素(LT4)替代疗法和维生素 E(VitE)补充对氧化应激诱导的心肌组织损伤和细胞凋亡的影响。

方法

雄性 Sprague-Dawley 大鼠分为五组:正常对照组、丙基硫氧嘧啶组(PTU 组)、LT4 治疗组(PTU+LT4 组)、维生素 E 治疗组(PTU+VitE 组)和联合治疗组(PTU+LT4+VitE 组)。测定血清和心肌中超氧化物歧化酶(SOD)活性和丙二醛(MDA)表达。用 TUNEL 法测定各组心肌细胞凋亡指数(AI)。

结果

PTU+VitE 和 PTU+LT4+VitE 组血清 SOD 水平明显高于 PTU 和 PTU+LT4 组(P<0.05)。PTU+LT4、PTU+VitE 和 PTU+LT4+VitE 组血清和心肌组织 MDA 水平明显低于 PTU 组(P<0.05)。PTU 和 PTU+VitE 组心肌细胞凋亡明显高于正常对照组(P<0.05),PTU+LT4 和 PTU+LT4+VitE 组明显低于 PTU 组(P<0.05)。

结论

本研究表明,左甲状腺素替代疗法和维生素 E 补充可改善甲状腺功能减退症大鼠的心肌细胞凋亡,其机制可能与改善甲状腺功能和减轻氧化应激有关。

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