Protective Role of Trans-chalcone against Kidney Injury Induced by High-Fat Diet: Exploring the Possible Involvement of FABP4 and Endoplasmic Reticulum Stress.

Authors

Elham Karimi-Sales, Khalil Hajiasgharzadeh, Parviz Shahabi, Mohammad Reza Alipour

Published in

Advanced biomedical research. Volume 15. Pages 56. Epub Sep 25, 2026.

Abstract

Obesity is a growing health concern, with an increasing prevalence. Overconsumption of a high-fat diet (HFD) is a risk factor for various diseases, including chronic kidney disease. Chronic HFD intake appears to be connected with ectopic deposition of lipids in the kidney, induction of endoplasmic reticulum (ER) stress, and renal dysfunction. Trans-chalcone is a flavonoid precursor with beneficial hepatoprotective, anti-inflammatory, anti-obesity, and anti-diabetic properties. Considering the role of fatty acid-binding protein 4 (FABP4) in triggering kidney diseases and inducing ER stress in response to lipids, the possible effects of Trans-chalcone and HFD intake on the renal expressions of FABP4 and indicators of ER stress were examined.
Twenty-one male Wistar rats were grouped into three groups: (1) control received 10% Tween 80, (2) HFD received a liquid HFD (10 mL/kg) and 10% Tween 80, and (3) HFD plus chalcone received a liquid HFD and Trans-chalcone (20 mg/kg). Administrations were performed by daily oral gavage for 42 consecutive days. Finally, fasting blood samples were used to evaluate Castelli's Risk Index-II (CRI-II). Additionally, the expression levels of FABP4, CAAT-enhancer-binding protein (C/EBP) homologous protein (CHOP), and glucose-regulated protein 78 (GRP78) in kidney samples were evaluated using real-time PCR.
Feeding with HFD significantly increased the atherogenic index (CRI-II) and the expression levels of FABP4, GRP78, and CHOP in the kidneys of animals. Conversely, Trans-chalcone significantly prevented these HFD-induced alterations.
Trans-chalcone can inhibit HFD-induced ER stress by suppressing FABP4 expression in the kidneys of rats fed the HFD.

PMID:
42891445
Bibliographic data and abstract were imported from PubMed on 18 Oct 2026.

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