Silibinin ameliorates the cardiovascular oxidative and inflammatory effects of type-2-diabetic rats exposed to air particulate matter

Abstract

Polycyclic Aromatic Hydrocarbons present in Diesel exhaust particle (DEP) has been established in different studies to cause deleterious toxic effects by inducing oxidative and pro-inflammatory effects. Diabetes is among the world’s top diseases. Silibinin (SIL) is a plant bioflavolignan with numerous health benefits. This study examined the effects of SIL on the oxidative and inflammatory status in the heart and aorta of type-2-diabetic (T2D) Wistar rats exposed to DEP. Type 2 diabetes was induced using streptozocin 45 mg/kg b.w of Wistar rats, which were later exposed to DEP (0.4 and 0.5 mg/kg) and post-treated with SIL. Another group of nondiabetic rats were administered DEP and later post-treated with 40 mg/kg SIL and the results were compared to the diabetic group. The results showed that DEP caused a significant (p < 0.001) increase in malondialdehyde and conjugated diene levels in the heart and aorta of T2D rats but was significantly (p < 0.001) attenuated by SIL. DEP induced interleukin 1 beta IL-1β, forkhead box protein 1 (FOXO1), heme-oxygenase HO-1, and decreased interleukin 10 (IL-10) gene expression, all of these were reversed in the presence of SIL. The expression of PI3K-AKT-GLUT4 (phosphatidylinositol-3-kinase, protein kinase B, glucose transporter 4) was significantly reduced by DEP in both tissues of T2D rats while SIL ameliorates against these effects. This indicates the potential of SIL to protect against DEP-induced cardiotoxicity in T2D subjects.

Graphical Abstract

Keywords:

• Diesel exhaust particles
• type-2-diabetes
• silibinin
• oxidative stress
• cardiovascular
• gene expression

Disclosure statement

No potential conflict of interest was reported by the authors.