Document Type : Original Research Article
Authors
1
Applied Cellular and Molecular Research Center, Kerman University of Medical Sciences, Kerman, Iran
2
Department of clinical Biochemistry, school of Medicine, Kerman university of medical sciences, Kerman, Iran
3
Noncommunicable Diseases Research Center, Bam University of Medical Sciences, Bam, Iran
4
Clinical Research Development Unit, Pastor Educational Hospital, Bam University of Medical Sciences, Bam, Iran
5
Physiology research center, Institute of neuropharmacology, Kerman university of medical sciences, Kerman, Iran
Abstract
Objective: Type 1 Diabetes (T1D) induces several consequences including hepatic damage resulting from oxidative stress and inflammation. The Nrf2/Keap1 pathway is crucial in oxidative stress signaling, and its modifications significantly influence health and illness. In this study, rats with T1D were used to test Citrullus colocynthis (CC) ability to reduce oxidative stress and inflammation in the diabetic liver.
Materials and Methods: Twenty-one male Wistar rats were assessed. Three groups—control (healthy rats), diabetes (received STZ), and diabetes with drug—were allocated at random to the rats. The CC fruits extract was administered to diabetic rats via gavage for 40 days. Oxidative stress indicators, including malondialdehyde (MDA), total antioxidant capacity (TAC), and superoxide dismutase (SOD), were determined. The ELISA method quantified liver cytokines, whereas western blotting evaluated the Nrf2/Keap1 pathway.
Results: The administration of CC in the Diabetes+Drug group dramatically reduced MDA levels while enhancing SOD activity and TAC levels in the liver. Following CC administration, Tumor necrosis factor alpha (TNF-α) levels decreased while rats with diabetes had higher amounts of interleukine-10 (IL-10) in their liver tissue. The CC administration could regulate the Nrf2/Keap1 pathway.
Conclusion: This study concluded that a daily administration of 200 mg/kg CC for 40 days can enhance liver function in diabetic subjects by controlling the Nrf2/Keap1 pathway and reducing oxidative stress and inflammation.
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