Figure 6.

Ameliorating effect of ASE on the CCl₄-induced systemic necroinflammation. (A–D) fold change in the gene expression 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 liver, brain, lung, and spleen tissues, respectively. (A) and (D) also show the fold change in the gene expression of the hepatic profibrotic mediators [collagen type I alpha one chain (COL1A1) and transforming growth factor (TGF)-β] and lung-specific pro-inflammatory cytokines [interleukin (IL)-1β and IL-8], respectively. Results are expressed as mean ± S.E of 7 animals. C control untreated rats, V olive oil (vehicle of CCl₄)-administered rats (0.5 ml/kg b.w., ip, 6 times), CCl₄ rats with systemic toxicity induced by CCl₄ injection (1 mL/kg b.w., ip, 6 times), CCl₄-ASE rats with systemic toxicity after their oral treatment with ASE (7.5 g/kg b.w.) for 10 days. ASE normal rats were administered only ASE (7.5 g/kg b.w.) for 10 days. Different letters refer to the significance at P < 0.05; CCl₄-ASE group was compared with the CCl₄ group, while V and ASE groups were individually compared with the C group.