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

**Authors:** Huda Rashid Atiyah, Sarmed H. Kathem, Surya M. Nauli

PMC · DOI: 10.3390/biom15111614 · 2025-11-17

## 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.

## Key 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.

## Linked entities

- **Proteins:** TNF (tumor necrosis factor), NFKB1 (nuclear factor kappa B subunit 1), FOS (Fos proto-oncogene, AP-1 transcription factor subunit), HAVCR1 (hepatitis A virus cellular receptor 1)
- **Chemicals:** citronellol (PubChem CID 7793)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}, Jun (Jun proto-oncogene, AP-1 transcription factor subunit) [NCBI Gene 16476] {aka AP-1, Junc, c-jun}, Havcr1 (hepatitis A virus cellular receptor 1) [NCBI Gene 171283] {aka KIM-1, TIM-1, Tim1, Timd1}, Nfkb1 (nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105) [NCBI Gene 18033] {aka NF-KB1, NF-kappaB, NF-kappaB1, p105, p50, p50/p105}
- **Diseases:** Sepsis (MESH:D018805), inflammatory cytokines (MESH:D000080424), decline in renal function (MESH:D060825), acute kidney inflammation (MESH:D058186), Renal Inflammation (MESH:D007249), kidney inflammation (MESH:D007674)
- **Chemicals:** creatinine (MESH:D003404), urea (MESH:D014508), Citronellol (MESH:C007078)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Figures

10 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12649931/full.md

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Source: https://tomesphere.com/paper/PMC12649931