Preliminary Study of Acute CoQ10 Effect in Etoricoxib-Induced Cardiac Biomarkers in Arthritic Rats

Cardiovascular complications are frequently observed as comorbidities in arthritis and may be exacerbated by prolonged use of selective cyclooxygenase-2 (COX-2) inhibitors such as Etoricoxib (ETO). Accumulating evidence suggests that oxidative stress and inflammation trigger these adverse cardiac outcomes. Coenzyme Q10 (CoQ10), a mitochondrial cofactor with antioxidant and anti-inflammatory properties, may offer cardioprotective benefits in this context. This study was designed to evaluate the role of CoQ10 in reducing cardiac markers elevated by ETO in rats with monosodium urate (MSU) induced arthritis. Arthritis was induced in male Wistar rats (n = 6 per group) via intradermal (i.d.) injection of MSU (3 days). ETO [(15 mg/kg, orally (p.o.)] either alone or in combination with CoQ10 (10 mg/kg, p.o.). Serum biochemical parameters creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), C-reactive protein (CRP), and tumour necrosis factor-alpha (TNF-α) were measured alongside myocardial levels of superoxide dismutase (SOD), and thiobarbituric acid reactive substances (TBARS). Cardiac tissue was examined histologically to evaluate structural alterations. ETO administered rats exhibited significant elevations in CK-MB, LDH, CRP, and TNF-α along with marked reductions in myocardial SOD (p < 0.05). These changes were validated by histopathological evidence of myocardial damage. CoQ10 co-administration significantly attenuated oxidative stress and inflammatory markers, restored antioxidant enzyme levels, and mitigated structural cardiac damage. The findings suggest that CoQ10 exerts partial but significant cardioprotection against ETO-induced cardiac markers in arthritic rats, likely through its modulatory effects on oxidative and inflammatory pathways.