Preventive effect of phytoglycoprotein (27 kDa) on inflammatory factors at liver injury in cadmium chloride‐exposed ICR mice

Abstract

Cadmium is one of the inflammation-related xenobiotics and has been regarded as a potent carcinogen. Gardenia jasminoides Ellis (GJE) has been used to cure inflammation in Korean folk medicine for a long time. The purpose of present study is the inhibitory effect of glycoprotein isolated from GJE (27 kDa) on inflammation mechanism in cadmium chloride-exposed ICR mice. We evaluated the activities of lactate dehydrogenase (LDH), alanine aminotransferase (ALT), and thiobarbituric acid-reactive substances (TBARS), activities of anti-oxidative enzymes [superoxide dismutase (SOD) and gluthathione peroxidase (GPx)], activities of c-Jun N-terminal protein kinase (JNK), heat shock protein 27 (Hsp27), activator protein (AP)-1, nuclear factor (NF)-κB and expression of inflammation-related mediators including tumor necrosis factor (TNF)-α and interleukin (IL)-6 in cadmium chloride-exposed ICR mice using immunoblot analysis, EMSA and RT-PCR. It notes that mice plasma was used to measure ALT, LDH, and TBARS after treatment with cadmium chloride alone or cadmium chloride under the pretreatment with GJE glycoprotein. Liver tissues were used to assess activities of anti-oxidant enzymes, SAPK/JNK, Hsp27, AP-1, NF-κB, TNF-α, and IL-6 in this study. The results obtained from this study revealed that GJE glycoprotein (10 mg/kg) decreased the levels of LDH, ALT and TBARS, whereas increased the activity of hepatic anti-oxidant enzymes (SOD and GPx) in cadmium chloride-exposed ICR mice. Moreover, it decreased the activity of JNK/AP-1, NF-κB, Hsp27, and pro-inflammatory cytokines (TNF-α and IL-6). Taken together, the results in this study suggest that GJE glycoprotein inhibits the expression of inflammation-related cytokines (TNF-α and IL-6) in cadmium chloride-exposed ICR mice.