Luteolin protects against diabetic cardiomyopathy by inhibiting NF-κB-mediated inflammation and activating the Nrf2-mediated antioxidant responses

Apr 23, 2019Phytomedicine : international journal of phytotherapy and phytopharmacology

Luteolin may protect the diabetic heart by reducing inflammation and boosting antioxidant defenses

AI simplified

Regenerative Health on OpenScience ↗PubMed ↗DOI ↗

Abstract

Luteolin significantly reduces high glucose-induced inflammation and oxidative stress in cardiomyocytes.

Luteolin inhibits the nuclear factor-kappa B (NF-κB) pathway, which is associated with inflammation.
Activation of the antioxidant nuclear factor-erythroid 2 related factor 2 (Nrf2) signaling pathway occurs with luteolin treatment.
These mechanisms lead to reduced expression of matrix proteins and cellular hypertrophy.
In mice with type 1 diabetes, luteolin prevents cardiac fibrosis, hypertrophy, and dysfunction.
There is a reduction in levels of inflammatory cytokines and oxidative stress biomarkers with luteolin administration.

AI simplified

BACKGROUND: Diabetes mellitus is a well-known risk factor for the development of heart failure. Inflammation and oxidative stress play a key role in the development of diabetic cardiomyopathy (DCM), and this nexus represents an attractive target to combat this disease. Naturally occurring flavonoid luteolin exhibits both anti-inflammatory and antioxidant activities in various systems.

HYPOTHESIS/PURPOSE: In this study, we aimed to investigate potential cardioprotective effects of luteolin in cultured cardiomyocytes and in mice with type 1 diabetes.

METHODS: C57BL/6 mice were intraperitoneal injection of streptozotocin (STZ) to induce DCM. High glucose (HG) was used to induce H9C2 cells injury in vitro. Cardiac fibrosis, hypertrophy, inflammation and oxidative stress were studied both in vitro and in vivo.

RESULTS: Our studies show that luteolin significantly reduces HG-induced inflammatory phenotype and oxidative stress in H9C2 cardiomyocytes. We found that the mechanisms involved inhibition of nuclear factor-kappa B (NF-κB) pathway and the activation of antioxidant nuclear factor-erythroid 2 related factor 2 (Nrf2) signaling pathway. Modulation of these pathways resulted in reduced expression of matrix proteins and cellular hypertrophy. Luteolin also prevented cardiac fibrosis, hypertrophy, and dysfunction in STZ-induced diabetic mice. These readouts were also associated with reduced levels of inflammatory cytokines and oxidative stress biomarkers.

CONCLUSION: Our results indicate that luteolin protects heart tissues in STZ-induced diabetic mice through modulating Nrf2-mediated oxidative stress and NF-κB-mediated inflammatory responses. These findings suggest that luteolin may be a potential therapeutic agent for DCM.

Full Text

Full text is available at the source.

View full text (XML) ↗View full text ↗

Luteolin protects against diabetic cardiomyopathy by inhibiting NF-κB-mediated inflammation and activating the Nrf2-mediated antioxidant responses

Abstract

Full Text

You found one interesting study. We’ll send the next 7.

what lands in your inbox each week: