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<p>Diabetes mellitus can apply its first adverse effects by developing endothelial dysfunction, which can progress to diabetic vasculopathy. This study was assessed the influence of melatonin on aortic reactivity to endothelin-1 (ET-1) in streptozotocin (STZ)-induced diabetic rats and to identify its mechanisms through calcium channels and endothelium-derived relaxing factors (EDRFs). This experimental study was carried out on rats randomly assigned to three groups: control, diabetic (induced by a single intraperitoneal dose of STZ), and diabetic treated with melatonin (30&#xa0;mg/kg for two weeks). After the rats were anesthetized and aortic rings were prepared, concentration-response curves to ET-1 were recorded alone and following preincubation with amlodipine (L-type calcium channel blocker), L-NAME (NOS inhibitor), and indomethacin (COX inhibitor). Histomorphic changes evaluated in all groups. Melatonin reduced vascular reactivity to ET-1 in the aorta of diabetic rats. Amlodipine did not reduce ET-1–induced contraction in diabetic group, but in the melatonin group, the inhibitory effect of amlodipine was restored (<i>P</i> &lt; 0.05). Pretreatment with L-NAME decreased the induced contraction in diabetic rats, unlike in the control group. Melatonin led to a contraction response close to that of the control group in diabetic rats. Diabetes increased aortic wall thickness and perinuclear space, and melatonin reversed these changes (<i>P</i> &lt; 0.05). The findings indicate that melatonin reduces vascular dysfunction and structural damage in diabetes by restoring L-type calcium channel sensitivity and modulating the balance of EDRFs, such as NO and prostanoids. These results highlight the potential of melatonin as an adjunct therapy for preventing diabetic vascular complications.</p>

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The role of melatonin in attenuation of vascular endothelin-1 reactivity via calcium channels and endothelial derived relaxing factors in STZ-induced diabetic aortic rats

  • 期刊论文

  • 发表日期：

    2026年4月22日

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  • Chrakhan J. Khdhir,
  • Ridha H. Hussein,
  • Ismail M. Maulood

摘要

Diabetes mellitus can apply its first adverse effects by developing endothelial dysfunction, which can progress to diabetic vasculopathy. This study was assessed the influence of melatonin on aortic reactivity to endothelin-1 (ET-1) in streptozotocin (STZ)-induced diabetic rats and to identify its mechanisms through calcium channels and endothelium-derived relaxing factors (EDRFs). This experimental study was carried out on rats randomly assigned to three groups: control, diabetic (induced by a single intraperitoneal dose of STZ), and diabetic treated with melatonin (30 mg/kg for two weeks). After the rats were anesthetized and aortic rings were prepared, concentration-response curves to ET-1 were recorded alone and following preincubation with amlodipine (L-type calcium channel blocker), L-NAME (NOS inhibitor), and indomethacin (COX inhibitor). Histomorphic changes evaluated in all groups. Melatonin reduced vascular reactivity to ET-1 in the aorta of diabetic rats. Amlodipine did not reduce ET-1–induced contraction in diabetic group, but in the melatonin group, the inhibitory effect of amlodipine was restored (P < 0.05). Pretreatment with L-NAME decreased the induced contraction in diabetic rats, unlike in the control group. Melatonin led to a contraction response close to that of the control group in diabetic rats. Diabetes increased aortic wall thickness and perinuclear space, and melatonin reversed these changes (P < 0.05). The findings indicate that melatonin reduces vascular dysfunction and structural damage in diabetes by restoring L-type calcium channel sensitivity and modulating the balance of EDRFs, such as NO and prostanoids. These results highlight the potential of melatonin as an adjunct therapy for preventing diabetic vascular complications.