Introduction:
Background: Diabetes stands as the predominant etiology behind end-stage kidney disease, commonly referred to as renal failure. The intricate interplay among oxidative stress, inflammation, and renal fibrotic changes in diabetes-induced nephropathy, particularly in instances involving and not involving the administration of mesenchymal stem cells (MSCs), remains a subject less explored in existing research.

Material and methods:
Methods: Twenty-four male Wistar rats (180 and 200 grams) were randomly assigned to one of three groups (n = 8). The control group received standard laboratory chow, and the groups with T2DM received a single dose of streptozotocin, 45 mg/kg, after three weeks of pretreatment with a high-fat diet (HFD). Rats with T2DM were split into the T2DM model group and Bone marrow (BM) mesenchymal stem cells (MSCs) treated group (T2DM+MSCs) eight weeks after DM was confirmed. BM-MSCs were injected systemically at 2 × 106 cells/rat doses.

Results:
Results: Diabetes significantly altered oxidative stress (MDA, SOD), inflammation (TNFα, IL-6), and kidney injury (KIM-1, NAGAL) biomarkers, a modulation that was mitigated by MSCs (p < 0.0001). Furthermore, diabetes-induced kidney fibrosis showed a noteworthy reduction in the presence of MSCs. A notable correlation emerged between body weight, systolic blood pressure (SBP), oxidative stress, inflammation, fibrosis, the PKC/NF-KB/STAT-3 axis, and hyperglycemia.

Conclusions:
Conclusions: Our results suggest that diabetes was associated with elevated oxidative stress, inflammation, biomarkers of kidney injury, upregulation of the renal PKC/NF-KB/STAT-3 pathway, and hypertension, all countered by MSCs intervention.