Abstract
The aim of the research is to explore the relationship between hyperthyroidism, iodine, antithyroid drugs (propylthiouracil) and vascular endothelial injury. In total, 136 SD rats were randomly allocated into the control group, the hyperthyroidism group, the hyperthyroidism propylthiouracil group, the hyperthyroidism low iodine group, the high iodine group, and the endothelial injury group. Rats were raised for 60 days. Afterward, indicators concerning endothelial damage were determined, including the von Willebrand Factor (vWF), thrombomodulin (TM), nitric oxide (NO), endothelin 1 (ET-1), and P-selectin, as well as the plant hemagglutinin sample type oxidized low-density lipoprotein receptor 1 (LOX-1) from the aorta and the number of endothelial progenitor cells (EPCs) in whole blood. The hyperthyroidism group had significantly higher values for vWF, TM, NO, ET-1, and P-selectin in serum and a higher number of EPCs in whole blood compared with the control group, similar to the LOX-1 expression in abdominal aorta. The hyperthyroidism low iodine group had significantly higher values for vWF, ET-1, and P-selectin in serum and a higher number of EPCs in whole blood compared with those of the control group, as was the case for LOX-1 expression in the abdominal aorta. The hyperthyroidism propylthiouracil group had significantly higher values for FT4 in the serum compared with those in the control group. The electron microscope showed that hyperthyroidism caused a certain degree of endothelial injury to the abdominal aorta in rats. Hyperthyroidism can damage the vascular endothelium and is a high-risk factor for cardio-cerebrovascular disease. Propylthiouracil could be used in the treatment of hyperthyroidism, thus protecting endothelial cells from damage.
Highlights
The aim of the research is to explore the relationship between hyperthyroidism, iodine, antithyroid drugs and vascular endothelial injury
The rats were divided into six groups according to weight: (1) control group, with normal diet and deionized water (50 μg/L iodine added), feeding for 60 days; (2) hyperthyroidism model group, with thyroxine tablets (25 mg/100 g, Shanghai Changcheng Pharmaceutical Co., Ltd.) continuous gavage for 30 days, the main ingredients of this product are made from the thyroid gland of food animals such as pigs, cattle, and sheep
Thyroid hormones include thyroxine (T4) and triiodothyronine (T3); after successful establishment of the model, thyroxine was stopped, and rats were supplied with normal diet and deionized water (50 μg/L iodine added, model group) every day; (3) hyperthyroidism PTU group, beginning with continuous gavage of thyroxine tablets (25 mg/100 g) for 30 days; after successful establishment of the model, thyroxine was stopped, and the rats were supplied with normal diet and deionized water (50 μg/L iodine added), followed by a daily dose of 5 mg/kg PTU gavage for 30 days (H + PTU group); (4) hyperthyroidism low iodine group, thyroxine tablets (25 mg/100 g), continuous gavage for 30 days
Summary
The aim of the research is to explore the relationship between hyperthyroidism, iodine, antithyroid drugs (propylthiouracil) and vascular endothelial injury. The hyperthyroidism low iodine group had significantly higher values for vWF, ET-1, and P-selectin in serum and a higher number of EPCs in whole blood compared with those of the control group, as was the case for LOX-1 expression in the abdominal aorta. Excess iodine exposure can increase oxidative stress, cause damage to vascular endothelial cells, and alter the expression of adhesion factors and the activity of nitric oxide www.nature.com/scientificreports synthase (NOS). These changes may explain the mechanisms underlying excess iodine-induced vascular injury[5]. This study explores the relationship between endothelial vascular damage and subsequent hyperthyroidism, and this study examined low iodine intake after hyperthyroidism, PTU treatment after hyperthyroidism, and high iodine intake as potential factors
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