Antibacterial and anti-atrophic effects of a highly soluble, acid stable UDCA formula in Helicobacter pylori-induced gastritis |
| |
Authors: | Thao Tran Dang Hien Ryu Ho-Cheol Yoo Seo-Hong Rhee Dong-Kwon |
| |
Affiliation: | aCollege of Pharmacy, Sungkyunkwan University, Su-won 440-746, South Korea bPrime Pharm Tech, Sungkyunkwan University Research Complex 2, Su-Won 440-746, South Korea |
| |
Abstract: | Helicobacter pylori is one of the main causes of atrophic gastritis and gastric carcinogenesis. Gastritis can also occur in the absence of H. pylori as a result of bile reflux suggesting the eradication of H. pylori by bile acids. However, the bile salts are unable to eradicate H. pylori due to their low solubility and instability at acidic pH. This study examined the effect of a highly soluble and acid stable ursodeoxycholic acid (UDCA) formula on H. pylori-induced atrophic gastritis. The H. pylori infection decreased the body weight, mitochondrial membrane potential and ATP level in vivo. Surprisingly, H. pylori-induced expression of malate dehydrogenase (MDH), a key enzyme in the tricarboxylic acid cycle, at both the protein and mRNA levels. However, the UDCA formula repressed MDH expression and increased the membrane potential thereby increasing the ATP level and body weight in vivo. Moreover, UDCA scavenged the reactive oxygen species (ROS), increased the membrane potential, and inhibited apoptosis in AGS cells exposed to H2O2 in vitro through the mitochondria-mediated pathway. Taken together, UDCA decreases the MDH and ROS levels, which can prevent apoptosis in H. pylori-induced gastritis. |
| |
Keywords: | Helicobacter Pylori-induced atrophic gastritis Ursodeoxycholic acid (UDCA) Mitochondria Reactive oxygen species |
本文献已被 ScienceDirect PubMed 等数据库收录! |
|