*2.7. Effect of OPs on The Hepatic Inflammatory Response (IL-1β, IL-6, TNF-α) in Cd-Exposed Mice*

Interleukin IL-1β and IL-6 are two stimulators of the hepatic synthesis of acute-phase proteins in the inflammatory response to stress and important biological markers of hepatic inflammation [25,26]. TNF-α is an important biological marker in substantial hepatic tissue damage [27]. As shown in Figure 5A–C, the mice in the Cd-exposed group have the highest level of hepatic inflammatory cytokines (IL-1β, IL-6, and TNF-α) (*p* < 0.01). OPs significantly attenuated Cd-induced the high level of hepatic IL-1β, IL-6, and TNF-α (*p* < 0.01 and *p* < 0.05, respectively). The results from quantitative reverse-transcription PCR analysis (qRT-PCR) manifested that OPs inhibited the expression of hepatic IL-1β, IL-6, and TNF-α in Cd-exposed mice (*p* < 0.01). These results revealed that the protection of OPs against Cd was associated with its attenuation of the Cd-induced hepatic inflammation in Cd-exposed mice.

**Figure 5.** Effect of OPs on inflammatory factor levels and mRNA expression on hepatic in Cd-exposed mice. (**A**) IL-1β level; (**B**) IL-6 level; (**C**) TNF-α level; (**D**–**F**) Hepatic mRNA expression levels of IL-1β, IL-6, and TNF-α in different groups. These data are expressed as the mean ± SEM, *n* = 6 in each group. Compared with the control group, \*\* *p* < 0.01; compared with the Cd group, # *p* < 0.05, ## *p* < 0.01.
