Atorvastatin suppresses Toll-like receptor 4 expression and NF-κB activation in rabbit atherosclerotic plaques

Area of Science:

• Cardiovascular Research
• Pharmacology
• Immunology

Background:

• Toll-like receptor 4 (TLR4) is implicated in atherosclerosis pathogenesis and inflammation.
• TLR4 is overexpressed in atherosclerotic lesions, driving inflammatory factor production.

Purpose of the Study:

• To evaluate atorvastatin's impact on TLR4 expression and NF-κB activation in rabbit atherosclerotic plaques.
• To explore atorvastatin's anti-atherosclerotic mechanisms beyond cholesterol reduction.

Main Methods:

• Atherosclerosis was induced in rabbits via a high-fat diet for 24 weeks.
• Atorvastatin treatment (2 mg/kg/day) was administered to a drug-treated group.
• TLR4 protein/mRNA and activated NF-κB (p65) levels were measured using Western blotting, qRT-PCR, and ELISA.

Main Results:

• Atorvastatin reduced TLR4 protein expression by 24.1% (p < 0.05) and mRNA by 46.9% (p < 0.01).
• NF-κB activation was significantly inhibited by 76.0% (p < 0.001) following atorvastatin treatment.
• These findings indicate a potent anti-inflammatory effect of atorvastatin in atherosclerotic plaques.

Conclusions:

• Atorvastatin exhibits anti-atherosclerotic activity by downregulating TLR4 and inhibiting NF-κB.
• The study suggests atorvastatin's therapeutic benefits extend beyond its lipid-lowering effects.
• These findings highlight TLR4 as a potential therapeutic target in atherosclerosis treatment.