Figure 4.

The improving activity of VVPF to CCl₄-induced brain oxidative stress and necroinflammation. (A) reactive oxygen species (ROS), total antioxidant capacity (TAC), and nitric oxide (NO) levels (B) thiobarbituric acid reactive substances (TBARS) level (C) myeloperoxidase (MPO) and superoxide dismutase (SOD) activities (D) glutathione peroxidase (GPX) activity and reduced glutathione (GSH) level. (E) gene expression fold change of the pro-inflammatory mediators [nuclear factor-kappa (NF-κ)B, inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, and tumor necrosis factor (TNF)-α] in the brain tissues. Results are expressed as mean ± S.E of 7 animals. C, Control untreated rats; CCl₄, rats with systemic toxicity induced by CCl₄ injection (1 mL/kg b.w., IP, 6 times); V, olive oil (vehicle of CCl₄)-injected rats (0.5 ml/kg b.w., IP, 6 times); CCl₄ + VVPF, rats with systemic toxicity after their gavage-fed VVPF (1.5 g/kg b.w.) for 10 days. VVPF, control rats gavage-fed only VVPF (1.5 g/kg b.w.) for 10 days. Different letters indicate the significance at p < 0.05; CCl₄ + VVPF group was compared with the CCl₄ group, while V and VVPF groups were independently compared with the C group. BHT butylated hydroxytoluene.