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Effect of Sodium Nitrite on the Genes Expression of Nrf2 and Prdx4 in the Isolated Pancreatic Islets of Type 2 Diabetic Rats
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S Jeddi    , A Ghasemi |
| Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, I.R. Iran. , ghasemi.asghar@gmail.com |
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Abstract: (127 Views) |
Introduction: Nitrite is a nitric oxide (NO) donor that increases insulin secretion from pancreatic islets in rats with type 2 diabetes (T2D). The underlying mechanism of this effect is the reduction of oxidative stress. This study aims to investigate the effect of nitrite on the expression of two genes involved in the oxidative stress process caused by T2D in the pancreatic islets of rats. Materials and Methods: T2D was induced in male rats by administering a high-fat diet along with a low dose of streptozotocin (25 mg/kg). The rats were divided into three groups (n=6 per group): control, T2D, and T2D+nitrite. The T2D+nitrite group received drinking water containing sodium nitrite (50 mg/L) for eight weeks. At the end of the study, mRNA levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and peroxiredoxin-4 (Prdx4) were measured in the isolated pancreatic islets. Results: In the pancreatic islets isolated from T2D rats, mRNA expression levels of Nrf2 and Prdx4 were significantly lower by 55% (P=0.005) and 77% (P<0.001), respectively, compared to the control group. Nitrite administration in T2D rats resulted in a 61% increase in Nrf2 expression (P=0.050) and a 94% increase in Prdx4 expression (P=0.009) in the isolated pancreatic islets. Conclusion: The beneficial effects of nitrite in reducing oxidative stress induced by T2D in the pancreatic islets of rats are associated with increased mRNA expression of Nrf2 and Prdx4.
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| Keywords: Nitrite, Nitric oxide, Nrf2, Oxidative stress, Pancreatic islets, Prdx4, Rat, Type 2 diabetes |
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Full-Text [PDF 917 kb]
(141 Downloads)
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Type of Study: Original |
Subject:
Physiology
Received: 2024/07/7 | Accepted: 2024/09/9 | Published: 2023/12/31
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