Hesperetin protects against diesel exhaust particles-induced cardiovascular oxidative stress and inflammation in Wistar rats

Inflammation Male 0301 basic medicine Hesperidin Cardiovascular System Lipids Rats Oxidative Stress 03 medical and health sciences Animals Particulate Matter Rats, Wistar Vehicle Emissions
DOI: 10.1007/s11356-022-19494-3 Publication Date: 2022-03-09T06:02:45Z
ABSTRACT
Air particulate matter exposure has been linked to cardiovascular and atherosclerosis as a result of increase oxidative stress and inflammatory response. This study aims to determine the effect of the use of hesperetin (HESP) as a therapeutic agent to mitigate the cardiovascular oxidative and pro-inflammatory effects of diesel exhaust particles in Wistar rats. DEP was collected from an Iveco cargo engine truck, and n-hexane fraction (hDEP) was obtained. Forty Wistar strains of male albino rats (6 weeks) were divided into 8 groups: control group received DMSO and CMC-Na; other groups received either n-hexane extract of DEP (0.064 or 0.640 mg/kg hDEP) or Standard Reference Material 2975 (0.064 mg/kg hSRM) in the presence or absence of 200 mg/kg HESP. Extracts were administered orally. Serum lipids, lipid peroxidation (LPO), conjugated dienes (CDs), and GSH levels were determined. Also, inflammatory cytokines, PCSK-9, LDL-receptor, and antioxidant genes expression were assessed by RT-PCR in both the heart and aorta. The molecular interaction of targeted proteins with HESP was assessed by the in silico approach. Extracts of DEP caused a significant (p < 0.001) increase in serum lipids but significantly decreased HDL-CHOL. It also increased CDs and MDA levels but decreased GSH levels. In addition, the particulate extracts caused a significant (p < 0.001) increase in pro-inflammatory genes expression in the heart and aorta but significantly decreased IL-10 and LDL-R gene expressions. Pre-treatment with hesperetin significantly reversed all these effects. This study shows that hesperetin has the ability to protect against DEP-induced oxidative stress and inflammation in the cardiovascular system.
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