Song Yeong Ok, Kim Mijeong, Woo Minji, Baek Jang-Mi, Kang Keon-Hee, Kim Sang-Ho, Roh Seong-Soo, Park Chan Hum, Jeong Kap-Seop, Noh Jeong-Sook
Department of Food Science and Nutrition and Kimchi Research Institute, Pusan National University, Busan 46241, Korea.
Yeongsan Skate Co. Ltd., Busan 48531, Korea.
Mar Drugs. 2017 Jun 15;15(6):178. doi: 10.3390/md15060178.
The protective effects of a chondroitin sulfate-rich extract (CSE) from skate cartilage against lipopolysaccharide (LPS)-induced hepatic damage were investigated, and its mechanism of action was compared with that of chondroitin sulfate (CS) from shark cartilage. ICR mice were orally administrated 200 mg/kg body weight (BW) of CS or 400 mg/kg BW of CSE for 3 consecutive days, followed by a one-time intraperitoneal injection of LPS (20 mg/kg BW). The experimental groups were vehicle treatment without LPS injection (NC group), vehicle treatment with LPS injection (LPS group), CS pretreatment with LPS injection (CS group), and CSE pretreatment with LPS injection (CSE group). Hepatic antioxidant enzyme expression levels in the CS and CSE groups were increased relative to those in the LPS group. In LPS-insulted hepatic tissue, inflammatory factors were augmented relative to those in the NC group, but were significantly suppressed by pretreatment with CS or CSE. Moreover, CS and CSE alleviated the LPS-induced apoptotic factors and mitogen-activated protein kinase (MAPK). In addition, CS and CSE effectively decreased the serum lipid concentrations and downregulated hepatic sterol regulatory element-binding proteins expression. In conclusion, the skate CSE could protect against LPS-induced hepatic dyslipidemia, oxidative stress, inflammation, and apoptosis, probably through the regulation of MAPK signaling.
研究了来自鳐鱼软骨的富含硫酸软骨素的提取物(CSE)对脂多糖(LPS)诱导的肝损伤的保护作用,并将其作用机制与来自鲨鱼软骨的硫酸软骨素(CS)进行了比较。将ICR小鼠连续3天口服给予200mg/kg体重(BW)的CS或400mg/kg BW的CSE,随后一次性腹腔注射LPS(20mg/kg BW)。实验组包括未注射LPS的载体处理组(NC组)、注射LPS的载体处理组(LPS组)、注射LPS的CS预处理组(CS组)和注射LPS的CSE预处理组(CSE组)。与LPS组相比,CS组和CSE组的肝抗氧化酶表达水平升高。在LPS损伤的肝组织中,炎症因子相对于NC组增加,但CS或CSE预处理可显著抑制炎症因子。此外,CS和CSE减轻了LPS诱导的凋亡因子和丝裂原活化蛋白激酶(MAPK)。此外,CS和CSE有效降低了血清脂质浓度,并下调了肝固醇调节元件结合蛋白的表达。总之,鳐鱼CSE可能通过调节MAPK信号通路来预防LPS诱导的肝血脂异常、氧化应激、炎症和凋亡。