Original article

Mesenchymal stem cell-derived secretome may attenuate nephrotoxicity by modulating cyclooxygenase-2 and caspase-3 levels in Wistar rats: an ELISA-based analysis

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Abstract

Aim: Nephrotoxicity is a major clinical concern because it can impair kidney function through inflammation and apoptosis. This study aimed to evaluate the effects of mesenchymal stem cell (MSC)-derived secretome on cyclooxygenase-2 (COX-2) and caspase-3 levels in a rat model of doxorubicin-induced nephrotoxicity.

Methods: A total of 24 male Wistar rats were randomly allocated into four groups: normal control (NC), nephrotoxicity control (TC), early MSC-derived secretome treatment (P1), and delayed MSC-derived secretome treatment (P2). Nephrotoxicity was induced using a single intraperitoneal injection of doxorubicin (10 mg/kg body weight). MSC-derived secretome was administered intravenously (0.15 mL) immediately after doxorubicin injection in the P1 group, and administered to the P2 group on day 5 after doxorubicin injection. All rats were euthanised on day 12. COX-2 and caspase-3 levels were measured using enzyme-linked immunosorbent assay (ELISA).

Results: A significant overall difference in COX-2 levels was observed among groups (p = 0.035). A strong, statistically significant positive correlation was observed between COX-2 and caspase-3 levels (r = 0.684, p = 0.002). The lowest COX-2 levels were found in the P1 group. No significant differences in caspase-3 levels were observed.

Conclusion: This study showed a significant overall difference in renal COX-2 levels among groups in a doxorubicin-induced nephrotoxicity rat model; however, Holm-adjusted post hoc comparisons did not confirm significant pairwise differences. Caspase-3 levels did not differ significantly among groups. These findings suggest that MSC-derived secretome may have potential anti-inflammatory effects, particularly when administered early after doxorubicin exposure, but further studies are required to confirm its effects on renal inflammation and apoptosis.

Keywords: apoptosis, doxorubicin, inflammation, kidney injury, regenerative medicine