Biochemical and biophysical research communications · 2026
Ameliorating effects of Coenzyme Q10 and its nanosuspension against cyclophosphamide-induced hepatoxicity in rats.
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Saeed Hager Y, Orabi Sahar H, Mansour Doaa A, Korany Reda M S, Alsofany Jihad M, Mousa Ahmed A
Аннотация
BACKGROUND: Coenzyme Q10 (CoQ10) is a natural antioxidant. In present study aims to evaluate the possible hepatoprotective effects against experimentally induced cyclophosphamide (CP) hepatotoxicity in rats.
METHODS: In total, 56 male albino rats were randomly distributed into 7 groups (n = 8). G1 (control saline); G2: (control corn oil group); G3: received CoQ10 (15 mg/kg orally) (100% purity) every 48 h for 4 weeks; G 4: administrated CoQ10-NS (15 mg/kg orally) every 48 h for 4 weeks; G5: received single injection of CP (150 mg/kg i.p) (1 g vial); G6: was treated with CoQ10 (15 mg/kg orally) every 48 h for 4 weeks after CP (150 mg/kg i.p); G7: was treated with CoQ10-NS (15 mg/kg orally) every 48 h for 4 weeks after CP (150 mg/kg i.p). Serum and hepatic tissue samples were obtained for biochemical analysis as well as histopathological evaluation.
RESULTS: The optimized formulation of CoQ10-NS (1.2% Poloxamer 407) showed particle size, polydispersity index, and zeta potential of 217.033 ± 2.650 nm, 0.274 ± 0.024, and -24.233 ± 0.777 mV, respectively, and excellent physical and chemical stability. Experimentally induced liver damage in the CP-injected rat group was evidenced by the increase of serum ALT and AST activities, elevated hepatic concentrations of malondialdehyde (MDA), decreased activity of hepatic glutathione peroxidase (GPx), and increased hepatic IL-6 and TNF-alpha levels. Alongside, CP induced histopathological changes with increased immune expression of Bax and caspase 3, and decreased Bcl-2 compared to the control groups. Meanwhile, CoQ10 and CoQ10-NS reversed all pathophysiological alterations induced by CP.
CONCLUSION: CoQ10 and CoQ10-NS showed ameliorative effects against the hepatic cytotoxicity induced by CP in rats, elucidating anti-inflammatory and anti-apoptotic properties with a marked superiority of CoQ10-NS to crude CoQ10 as a result of nanosizing and enhanced bioavailability.
METHODS: In total, 56 male albino rats were randomly distributed into 7 groups (n = 8). G1 (control saline); G2: (control corn oil group); G3: received CoQ10 (15 mg/kg orally) (100% purity) every 48 h for 4 weeks; G 4: administrated CoQ10-NS (15 mg/kg orally) every 48 h for 4 weeks; G5: received single injection of CP (150 mg/kg i.p) (1 g vial); G6: was treated with CoQ10 (15 mg/kg orally) every 48 h for 4 weeks after CP (150 mg/kg i.p); G7: was treated with CoQ10-NS (15 mg/kg orally) every 48 h for 4 weeks after CP (150 mg/kg i.p). Serum and hepatic tissue samples were obtained for biochemical analysis as well as histopathological evaluation.
RESULTS: The optimized formulation of CoQ10-NS (1.2% Poloxamer 407) showed particle size, polydispersity index, and zeta potential of 217.033 ± 2.650 nm, 0.274 ± 0.024, and -24.233 ± 0.777 mV, respectively, and excellent physical and chemical stability. Experimentally induced liver damage in the CP-injected rat group was evidenced by the increase of serum ALT and AST activities, elevated hepatic concentrations of malondialdehyde (MDA), decreased activity of hepatic glutathione peroxidase (GPx), and increased hepatic IL-6 and TNF-alpha levels. Alongside, CP induced histopathological changes with increased immune expression of Bax and caspase 3, and decreased Bcl-2 compared to the control groups. Meanwhile, CoQ10 and CoQ10-NS reversed all pathophysiological alterations induced by CP.
CONCLUSION: CoQ10 and CoQ10-NS showed ameliorative effects against the hepatic cytotoxicity induced by CP in rats, elucidating anti-inflammatory and anti-apoptotic properties with a marked superiority of CoQ10-NS to crude CoQ10 as a result of nanosizing and enhanced bioavailability.