Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapieJul 3, 2021

Phenethyl isothiocyanate reduces diabetic kidney damage by changing harmful sugar, oxidation, and inflammation signals in diabetic rats

GLP-1 Therapies Weekly Brief ↗PubMed ↗DOI ↗

Updated Mar 30, 2026

Abstract

PEITC (3, 10, and 30 mg/kg) significantly improved kidney and liver functions in a rat model of diabetic nephropathy.

PEITC treatment led to improved renal histopathological features and reduced tissue fibrosis.
Blood glucose levels were decreased in rats treated with PEITC compared to the diabetic nephropathy control group.
PEITC alleviated renal damage by modulating glycation and oxidative stress, as well as the inflammatory response.
The treatment activated glyoxalase 1, reducing the expression of advanced glycation end products and their receptor.
PEITC increased the activity of protective proteins associated with antioxidant responses while decreasing repressor protein levels.
The anti-inflammatory effects of PEITC included downregulation of key inflammatory markers related to the NLRP3 inflammasome.

Simplified

Diabetic nephropathy (DN) is a diabetic complication characterized by disruption of renal microvasculature, reactive oxygen species accumulation and increased inflammation, all of which contribute to renal injury. Phenethyl isothiocyanate (PEITC) is a naturally occurring isothiocyanate well known for its antioxidant and anti-inflammatory effects, yet its reno-preventive effects against DN has not been investigated. The current study looked into the in vivo reno-protective effects of PEITC in STZ-induced DN in rats. PEITC (3, 10 and 30 mg/kg) was administered orally for 8 weeks post DM establishment. PEITC treatment significantly improved kidney and liver functions, renal histopathological features, tissue fibrosis, macrophage infiltration and blood glucose levels compared to DN control. Mechanistically, PEITC treatment alleviated DN-induced renal damage via modulating glycation and oxidative stresses and inflammatory response. As such, PEITC activated glyoxalase 1 (GLO1) that induced a retraction in renal tissue expression of advanced glycation end products (AGEs) and its receptor (RAGE). PEITC activated nuclear erythroid 2-related factor 2 (Nrf2) and increased expression of its downstream targets, hemeoxygenase-1 (HO-1) and gamma glutamate-cysteine (γ-GCS). Additionally, PEITC treatment decreased the expression of Nrf2 repressor protein, keap1. The anti-inflammatory effect of PEITC was driven, at least in part, via reducing the NLRP3 inflammasome activation as indicated by down regulation of NLRP3, TXNIP, capsase-1 and IL-1β, TNF-alpha and IL-6. In conclusion; PEITC attenuated DN progression in a dose dependent manner mainly via interruption of AGE/RAGE and NLPR3/TXNIP/NrF2 crosstalk.

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Phenethyl isothiocyanate reduces diabetic kidney damage by changing harmful sugar, oxidation, and inflammation signals in diabetic rats

Abstract

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