Biotechnology Research Institute, Center for the Control of Animal Hazards Using Biotechnology (BK21), Chonnam National University, Gwang-ju, South Korea.
J Cell Biochem. 2011 Feb;112(2):694-703. doi: 10.1002/jcb.22980.
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.
镉是一种与炎症相关的异生物质，已被认为是一种强有力的致癌物质。栀子（GJE）长期以来一直被韩国民间医学用于治疗炎症。本研究的目的是研究从栀子（27 kDa）中分离得到的糖蛋白（27 kDa）对氯化镉暴露的 ICR 小鼠炎症机制的抑制作用。我们评估了乳酸脱氢酶（LDH）、丙氨酸氨基转移酶（ALT）和硫代巴比妥酸反应物质（TBARS）的活性、抗氧化酶[超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPx）]的活性、c-Jun N-末端蛋白激酶（JNK）、热休克蛋白 27（Hsp27）、激活蛋白（AP）-1、核因子（NF）-κB 的活性以及用免疫印迹分析、EMSA 和 RT-PCR 检测氯化镉暴露的 ICR 小鼠中炎症相关介质包括肿瘤坏死因子（TNF）-α和白细胞介素（IL）-6 的表达。值得注意的是，在用氯化镉单独处理或用 GJE 糖蛋白预处理后，用氯化镉处理的 ICR 小鼠的血浆用于测量 ALT、LDH 和 TBARS。本研究还用于评估肝组织中抗氧化酶、SAPK/JNK、Hsp27、AP-1、NF-κB、TNF-α和 IL-6 的活性。本研究结果表明，GJE 糖蛋白（10 mg/kg）降低了氯化镉暴露的 ICR 小鼠的 LDH、ALT 和 TBARS 水平，而增加了肝抗氧化酶（SOD 和 GPx）的活性。此外，它降低了 JNK/AP-1、NF-κB、Hsp27 和促炎细胞因子（TNF-α和 IL-6）的活性。总之，本研究结果表明，GJE 糖蛋白抑制了氯化镉暴露的 ICR 小鼠中炎症相关细胞因子（TNF-α和 IL-6）的表达。
