The effect of vitamin C administration on gastric acid secretion and ulcer in diabetic rats was studied. Vitamin C (200mg/kg b.w.) was administered to both streptozotocin-induced diabetic and control groups orally for 28 days. Gastric acid secretion was measured and ulcer was induced using ethanol. Histological changes were observed in the stomach. Basal and stimulated acid secretion in diabetic control rat was significantly () decreased when compared to vitamin C-treated diabetic group and control. Administration of vitamin C significantly () increased the histamine-stimulated gastric acid secretion in diabetics than control while reduction in gastric secretion by ranitidine was similar compared with control. Vitamin C treatment significantly () reduced ulcer index in diabetic group and increased mucus weight when compared with diabetic group which was also confirmed with photomicrographs. The mean body weight of diabetic rats treated with vitamin C was comparable to the control. The blood glucose level was significantly () reduced in diabetic group given vitamin C (mMol/L) compared to the diabetic control (g). It is concluded that vitamin C is beneficial in improving gastric acid secretion and protects against ulceration in streptozotocin-induced diabetes mellitus in rats due to its antioxidant potential.

Objectives: Gongronema latifolium leaves have been used in folklore medicine to manage diabetes mellitus and alleviate dyspepsia. This study aimed to provide a pharmacological basis to the medicinal use of Gongronema latifolium as an antidiabetic and antiulcerogenic agent in diabetes mellitus.

Gentamicin-induced nephrotoxicity (GIN) remains a significant clinical challenge due to its association with oxidative stress, inflammation, and mitochondrial dysfunction. Despite its effectiveness as an aminoglycoside antibiotic for treating Gram-negative bacterial infections, gentamicin’s nephrotoxic potential limits its clinical use, affecting 10–20% of patients. In response to these challenges, naringenin, a flavonoid with potent antioxidant and anti-inflammatory properties, has emerged as a promising therapeutic agent for mitigating renal damage. This narrative review explores the multifaceted mechanisms underlying naringenin’s nephroprotective effects, including its ability to neutralize reactive oxygen species (ROS), modulate inflammatory pathways, and enhance cellular repair mechanisms through pathways such as PI3K/Akt and MAPK. Both in vitro and in vivo studies support the capability of naringenin to counteract gentamicin-induced nephrotoxicity by preserving renal function, reducing oxidative stress, and reducing inflammation. While preclinical evidence is robust, further clinical research is essential to establish its efficacy, safety, and optimal dosing in nephrotoxic contexts. This review synthesizes existing data and highlights the need for continued investigation into naringenin as a potential adjunctive therapy in the management of nephrotoxicity.