Study on the gastroprotective effects of Corbicula fluminea in gastric mucosal cells

• Main Authors: Huang, Chien-Hua, 黃芊華
• Other Authors: Chen, Yu-Kuo
• Format: Others
• Language: zh-TW
• Published: 2018
• Online Access: http://ndltd.ncl.edu.tw/handle/7985ck

碩士 === 國立屏東科技大學 === 食品科學系所 === 106 === Gastric mucosal injury is a common disease, and gastric cancer is often derived from gastric damage, so gastric mucosal injury is an important issue that should not be underestimated. Gastric mucosal injury caused by stress, excessive drinking, gastric acid, Helicobacter pylori, overuse of non-steroidal anti-inflammatory drugs (NSAIDs) and other factors because these factors cause gastric mucosal mechanism imbalance. Among them, over administration of NSAIDs is the most common type of gastric mucosal ulcer. Indomethacin, a kind of NSAIDs, is always used to treat inflammatory diseases, such as rheumatoid arthritis and gout, but its side effect is causing gastric mucosal damage. The research showed that Corbicula fluminea has the effect of protecting the liver and improving sight. Studies have showed that the clams have the physiological activity of inhibiting liver cancer, anti-hypertension and anti-oxidation. However, there are few studies on the protection of gastric mucosal cells by clams. Therefore, the purpose of this study was to investigate the protective effect of clams extract in gastric mucosal cells. C. fluminea was first extracted with water to obtain water extract of clam (WEC). The cytotoxicity test on RGM1 cell by WEC treatment to select a range of doses that are not toxic. RGM1 cells were seeded in medium containing 0.8 mM indomethacin. The results showed that indomethacin treatment can cause damage to RGM-1 cell, and the cell viability decreased to 37%. Pre-treatment of 15.63 μg/mL of WEC for two hours significantly restored the cell viability of RGM-1 cells to 64%, and showed a dose-dependent effect. Further experimental results showed that indomethacin increases intracellular reactive oxygen species. However, the production of ROS in RGM1 cells were significantly decreased with treatment of WEC at 62.5 μg/mL and in a dose dependent manner. The protein expression of NF-κB in the nucleus significantly increased in indomethacin-induced group by western blot analysis. However, the WEC group inhibited the nuclear translocation of NF-κB compared with indomethacin-induced group. Therefore, the protein expression of cyclooxygenase-2 (COX-2) and inflammatory factor, iNOS in the WEC group decreased compared with the indomethacin-induced group. These finding suggest that that WEC can prevent indomethacin-induced gastric mucosal injury by reducing the generation of ROS to further inhibit the nuclear translocation of NF-κB and transcription into inflammatory cytokines.