Citronellol Reduces Sepsis-Induced Renal Inflammation via AP-1/NF-κB/TNF-α Pathway

TL;DR

Citronellol, a natural compound, reduces kidney inflammation in sepsis by targeting specific inflammatory pathways.

Contribution

This study demonstrates citronellol's anti-inflammatory effects in a mouse model of sepsis-induced kidney injury.

Findings

Citronellol reduced serum urea and creatinine levels in sepsis-induced mice.

Citronellol suppressed pro-inflammatory cytokines TNF-α, NF-κB, and AP-1.

Citronellol improved renal function and reduced inflammation in a mouse model of sepsis.

Abstract

Sepsis is characterized by the over-production of pro-inflammatory cytokines. Cecal ligation and puncture (CLP) is a well-accepted model for recreating sepsis-induced renal injury in mice. The current study investigates how citronellol, a naturally occurring substance with a variety of biological characteristics, can prevent acute kidney inflammation brought on by CLP. In the CLP mouse model, citronellol was administered orally at doses of 50 and 100 mg/kg. Serum levels of creatinine and urea were used as markers of renal function, and the Murine Sepsis Score (MSS) was used to assess the severity of sepsis. According to our findings, CLP caused a decline in renal function, as shown by higher serum urea and creatinine levels in comparison to control mice. Nevertheless, administering citronellol as pretreatment at doses of 50 and 100 mg/kg alleviated the deterioration in renal functions. Citronellol decreased levels of serum urea and creatinine. Citronellol demonstrated an anti-inflammatory effect by reducing pro-inflammatory cytokines (TNF-α, NF-κB, AP-1) and KIM-1. Overall, our study suggests that citronellol holds a promise as a potential therapeutic agent for mitigating kidney inflammation.

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