ISSN 2326-7275
International Journal of Anatomy and Physiology ISSN 2326-7275 Vol. 14 (6), pp. 001-012, June, 2026.
Full Length Research Paper
Inflammatory Mediators, Apoptosis, and Nitric Oxide in Type II Diabetes Mellitus: Exacerbating Renal Ischemia-Reperfusion Injury
Mahmoud M. Gabr1, Abdel-Aziz M. Hussein2*, Iman O. Sherif3, Sousou I. Ali3 and Hoda E. Mohamed3
1Urology and Nephrology Center, Mansoura, Egypt.
2Department of Physiology, Faculty of Medicine, Mansoura University, Cairo Egypt.
3Department of Biochemistry, Faculty of Pharmacy, Zagazig University, Zagazig, Egypt.
Accepted 21 September, 2025
Diabetes mellitus (DM) especially type II is a major health problem and diabetic nephropathy is the main cause of end stage renal disease (ESRD). Renal ischemia/reperfusion (I/R) injury is common in diabetic patients. Recent studies reported increased vulnerability of kidney to I/R injury in diabetic rats. Mechanisms behind this increased vulnerability not fully understood. The present study investigated the effect of acute ischemia for 45 min on proinflammatory cytokines, apoptotic markers, and nitric oxide (NO) in a rat model of type II diabetes. Sixty male Sprague Dawley rats were divided into 4 groups (n = 15, each); Group I: Normal rats, Group II: Normal rats underwent left renal ischemia for 45 min, Group III: diabetic rats without renal ischemia, Group IV: diabetic rats underwent left renal ischemia for
45 min. Blood and kidney samples were taken 24 h after ischemia. Serum glucose, fructosamine, creatinine, TNFa, as well as the expression of TGFβ, NFkappaB, iNOS, survivin, and Bcl2 in kidney tissue was measured. Type II DM caused significant increase in serum glucose, fructosamine, creatinine, and TNFa and expression of TGFβ, NFkB and iNOS in renal tissue (P < 0.001). Also, DM caused significant increase in apoptotic cell death with increase in Bcl-2 expression and decreased survivin in kidney. 45 min ischemia in diabetic rats caused more significant increase in serum TNF-a and expression of TGF-β, NF-kappa B and iNOS (P < 0.001). Also; there was a positive correlation between blood glucose and TNFa, TGFβ, NFkB and iNOS with negative correlation with survivin (P < 0.01). Type II DM render the kidney more susceptible to ischemic injury. Proinflammatory cytokines TNF-a, TGFβ, and NFkB and iNOS as well as Bcl2 and survivin may contribute to the enhanced renal ischemic injury in type II DM. Also, hyperglycaemia may be involved in hypersensitivity of kidney to ischemic injury in DM.
Key words: Diabetes, kidney, ischemia, apoptosis, TNFalpha, TGFbeta, NFkB, iNOS, Bcl-2, surviving.