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Mesenchymal stem cell-derived secretome may attenuate nephrotoxicity by modulating cyclooxygenase-2 and caspase-3
Dedy Syahrizal1, Rika Farhana2, Jufriady Ismy3
1Department of Biochemistry, Faculty of Medicine, Universitas Syiah Kuala, Aceh, Indonesia.
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.
Insights
Mesenchymal stem cell secretome may reduce kidney inflammation markers in rats with doxorubicin-induced nephrotoxicity. Early secretome treatment showed the lowest cyclooxygenase-2 (COX-2) levels, suggesting potential anti-inflammatory benefits.
Area of Science:
- Nephrology
- Regenerative Medicine
- Biomedical Research
Background:
- Nephrotoxicity is a significant clinical challenge, often leading to kidney dysfunction via inflammation and apoptosis.
- Doxorubicin is a common chemotherapeutic agent known to induce nephrotoxicity.
Purpose of the Study:
- To investigate the therapeutic potential of mesenchymal stem cell (MSC)-derived secretome in mitigating doxorubicin-induced nephrotoxicity in rats.
- To evaluate the impact of MSC secretome on key markers of kidney injury: cyclooxygenase-2 (COX-2) and caspase-3.
Main Methods:
- A rat model of doxorubicin-induced nephrotoxicity was established.
- Rats were divided into four groups: normal control, nephrotoxicity control, early MSC secretome treatment, and delayed MSC secretome treatment.
- MSC secretome was administered intravenously at different time points post-doxorubicin induction.
- Renal COX-2 and caspase-3 levels were quantified using enzyme-linked immunosorbent assay (ELISA).
Main Results:
- A significant overall difference in renal COX-2 levels was detected among the experimental groups.
- The early MSC secretome treatment group exhibited the lowest COX-2 levels.
- A significant positive correlation was found between COX-2 and caspase-3 levels.
- No significant differences in caspase-3 levels were observed across the groups.
Conclusions:
- MSC-derived secretome demonstrated a potential to modulate renal COX-2 levels in a doxorubicin-induced nephrotoxicity model.
- Early administration of MSC secretome may offer protective anti-inflammatory effects.
- Further research is warranted to fully elucidate the mechanisms and confirm the efficacy of MSC secretome in preventing renal inflammation and apoptosis.
