# The preventive effect of chlorogenic acid on cisplatin-induced acute kidney injury in mice

**Authors:** Zheng Hongya, Duan Yichang, Zhong Zheng, Zhu Yanzhu, Niu Wei, Huang Caoxing, Yin Baishuang

PMC · DOI: 10.3389/fvets.2026.1763548 · Frontiers in Veterinary Science · 2026-02-19

## TL;DR

Chlorogenic acid helps protect mice from kidney damage caused by cisplatin, a chemotherapy drug, by reducing inflammation and oxidative stress.

## Contribution

This study shows that chlorogenic acid can prevent cisplatin-induced kidney injury in mice through antioxidant and anti-inflammatory mechanisms.

## Key findings

- Chlorogenic acid reduced kidney injury markers like creatinine and BUN in mice.
- It enhanced antioxidant enzyme activities and increased Nrf2 and GCLC protein expression.
- Inflammatory cytokines were reduced, and kidney structure was preserved with CGA treatment.

## Abstract

Acute kidney injury (AKI) is a common clinical syndrome. Chlorogenic acid (CGA) is a natural polyphenol with antioxidant and anti-inflammatory properties. In this study, 60 male Kunming mice were randomly assigned to 6 groups: Control (CON), Cisplatin (CIS), CGA, CIS + CGA, CIS + furosemide (FUR), and FUR. Kidney injury markers, inflammatory indicators, antioxidant enzyme activities, oxidative products, antioxidant proteins, and kidney morphology were assessed using ELISA, histology, and Western blot. Preventive CGA supplementation significantly reduced levels of creatinine (Cr), BUN, KIM-1, and MDA, while restoring the enzymatic activities of SOD, GSH-Px, CAT, and T-AOC. CGA also increased the expression of Nrf2 and GCLC proteins and decreased the expression of Keap1 protein. Levels of IL-1β, IL-2, and IL-6 were reduced, while IL-10 levels were elevated. These results indicate that preventive CGA supplementation effectively mitigates CIS-induced AKI by enhancing antioxidant capacity, attenuating inflammatory responses, and ameliorating kidney structural damage.

## Linked entities

- **Proteins:** GABPA (GA binding protein transcription factor subunit alpha), GCLC (glutamate-cysteine ligase catalytic subunit), KEAP1 (kelch like ECH associated protein 1)
- **Chemicals:** chlorogenic acid (PubChem CID 1794427), cisplatin (PubChem CID 5460033), furosemide (PubChem CID 3440), GSH-Px (PubChem CID 168010211), IL-2 (PubChem CID 51397006), IL-6 (PubChem CID 165368475), IL-10 (PubChem CID 146070)
- **Diseases:** acute kidney injury (MONDO:0002492), AKI (MONDO:0002492)

## Full-text entities

- **Genes:** Il10 (interleukin 10) [NCBI Gene 16153] {aka CSIF, If2a, Il-10}, Il2 (interleukin 2) [NCBI Gene 16183] {aka Il-2}, Pphln1 (periphilin 1) [NCBI Gene 223828] {aka CR, HSPC206, HSPC232}, Gclc (glutamate-cysteine ligase, catalytic subunit) [NCBI Gene 14629] {aka D9Wsu168e, GLCL-H, Ggcs-hs, Glclc}, Mul1 (mitochondrial ubiquitin ligase activator of NFKB 1) [NCBI Gene 68350] {aka 0610009K11Rik, Gide, Tnrip-1}, Tlr4 (toll-like receptor 4) [NCBI Gene 21898] {aka Lps, Ly87, Ran/M1, Rasl2-8}, Keap1 (kelch-like ECH-associated protein 1) [NCBI Gene 50868] {aka INRF2, mKIAA0132}, Havcr1 (hepatitis A virus cellular receptor 1) [NCBI Gene 171283] {aka KIM-1, TIM-1, Tim1, Timd1}, Cat (catalase) [NCBI Gene 12359] {aka 2210418N07, Cas-1, Cas1, Cs-1}, Nfe2l2 (nuclear factor, erythroid derived 2, like 2) [NCBI Gene 18024] {aka Nrf2}, 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}, Il1b (interleukin 1 beta) [NCBI Gene 16176] {aka IL-1beta, Il-1b}, Il1 (interleukin 1 complex) [NCBI Gene 111343] {aka Il-1}, Il6 (interleukin 6) [NCBI Gene 16193] {aka Il-6}, Cish (cytokine inducible SH2-containing protein) [NCBI Gene 12700] {aka CIS-1, CIS1, Cis, F17, F23, SOCS}, Cul3 (cullin 3) [NCBI Gene 26554] {aka KIAA0617}
- **Diseases:** CKD (MESH:D012080), toxicity (MESH:D064420), reperfusion injury (MESH:D015427), Kidney injury (MESH:D007674), Oliguria (MESH:D009846), tubular injury (MESH:D000230), electrolyte disturbances (MESH:D014883), chronic kidney disease (MESH:D051436), Inflammatory (MESH:D007249), fibrosis (MESH:D005355), mitochondrial damage (MESH:D028361), metabolic disorders (MESH:D008659), ischemia (MESH:D007511), metabolic alkalosis (MESH:D000471), AKI (MESH:D058186)
- **Chemicals:** FUR (MESH:D005665), sodium arsenite (MESH:C017947), reactive nitrogen species (MESH:D026361), uranyl acetate (MESH:C005460), MDA (MESH:D008315), epoxy resin (MESH:D004853), AOC (-), H2O2 (MESH:D006861), CIS (MESH:D002945), hematoxylin (MESH:D006416), indoxyl sulfate (MESH:D007200), glutaraldehyde (MESH:D005976), eosin (MESH:D004801), PVDF (MESH:C024865), CGA (MESH:D002726), formalin (MESH:D005557), Cr (MESH:D003404), polyphenol (MESH:D059808), glutathione (MESH:D005978), lipid (MESH:D008055), urea nitrogen (MESH:C530477), LPS (MESH:D008070), xylene (MESH:D014992), MDA (MESH:D015104), polyacrylamide (MESH:C016679), paraffin (MESH:D010232), phosphate (MESH:D010710), osmium tetroxide (MESH:D009993), copper (MESH:D003300), sodium dodecyl sulfate (MESH:D012967), ethanol (MESH:D000431), D-galactose (MESH:D005690), Epon 812 (MESH:C004875), water (MESH:D014867), free radicals (MESH:D005609)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]
- **Mutations:** rs751402, glutamate-cysteine

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## References

39 references — full list in the complete paper: https://tomesphere.com/paper/PMC12960156/full.md

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Source: https://tomesphere.com/paper/PMC12960156