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Backgroud

Kidney transplantation is the optimal treatment for end-stage renal disease, yet acute rejection remains a significant challenge to the survival rates of grafts. Ischemia-reperfusion injury (IRI) can initiate an inflammatory response that severely damages the transplanted kidney.

Methods

The APJ/apelin system has been shown to play an anti-inflammatory role across various domains, and in this study, we utilized apelin-13 in a rat kidney transplantation model to investigate its effects on IRI-related inflammation.

Results

Our findings indicate that apelin predominantly localizes in the renal cortex, and following kidney transplantation, there was destruction of tissue structure and an inflammatory response targeting the transplanted kidney. The administration of apelin-13 led to improved kidney function, reduced organizational structure damage, and lower injury and apoptosis indices compared to the control group. Notably, following the administration of apelin-13, the expression levels of pro-inflammatory cytokines, such as TNF-α, IL-6, and IL-1β, were reduced in comparison to the model control group, as determined by immunofluorescence, western blot, and ELISA Manuscript File Click here to view linked References assays. Furthermore, the extent of CD3 T cell infiltration was lower relative to that in the model control group. We specifically examined the classical inflammation signaling pathway, NF-κB. Our results show that, compared to the model group, the administration of apelin-13 reduced the expression of NF-κB signaling pathway proteins, as evidenced by both immunohistochemistry and western blot analyses.

Conclusions

In conclusion, apelin-13 appears to reduce the inflammatory response to ischemia-reperfusion injury following kidney transplantation, partly through the NF-κB signaling pathway.