Effect of anthocyanins on expression of matrix metalloproteinase-2 in naproxen-induced gastric ulcers

Abstract

Non-steroidal anti-inflammatory drugs cause gastric ulceration through a number of mechanisms including inhibition of PG synthesis, generation of reactive oxygen species (ROS) and induction of apoptosis. Recently, matrix metalloproteinases (MMP) have been suggested to play a crucial role in these mechanisms. The present study investigated the protective effect of anthocyanins isolated from black rice bran (Heugjinjubyeo) against naproxen-induced gastric mucosal injury in rats. The oral administration of anthocyanins (5, 25 or 50 mg/kg body weight) showed significant protection against naproxen (80 mg/kg body weight)-induced gastric ulcer and inhibited lipid peroxidation in the gastric mucosa. In addition, pretreatment with anthocyanins resulted in a significant increase in the activities of radical-scavenging enzymes such as superoxide dismutase, catalase and glutathione peroxidase. Also biochemical and zymographic analyses suggested that the administration of anthocyanins gives a significant protection against naproxen-induced gastric antral ulcer through scavenging ROS and regulation of matrix metalloproteinase-2 (MMP-2) activity. The results of intracellular radical activation show that anthocyanins suppress the generation of intracellular ROS and attenuate the suppression of MMP-2 activity by naproxen. These results suggest that anthocyanins extracted from black rice may offer potential remedy of gastric antral ulceration.

Role of allelic genes of matrix metalloproteinases and their tissue inhibitors in the risk of peptic ulcer disease development

“…Some studies have shown that expression of MMP 2 and MMP 9 is highly pronounced in tumor tissues as compared with normal tissue and that polymorphisms rs2285052 of gene MMP 2 and rs3918242 of gene MMP 9 play an important role in the development of gastric ulcers and stomach cancer [27,28]. MMP 9, one of the most important MMPs, is known for degrading the extracellular matrix and basement membrane, thereby contributing to disease progres sion of various cancers by increasing the migration, invasion, metastasis, and angiogenesis [29].…”

Shikonin Induces Apoptotic Cell Death via Regulation of p53 and Nrf2 in AGS Human Stomach Carcinoma Cells

“…Malondialdehyde (MDA) levels were measured using a commercial assay kit (Cayman chemical, Ann Arbor, MI, USA) according to the manufacturer’s instructions. Proteins were determined by the method of Bradford (Kim et al ., 2011b). …”

Dual Alpha2C/5HT1A Receptor Agonist Allyphenyline Induces Gastroprotection and Inhibits Fundic and Colonic Contractility

“…Although a detailed analysis of the peripheral factors involved in the mucosal protection was above the scope of the present study, we addressed the question of whether allyphenyline is able to counteract oxidative stress, an important factor in the pathomechanism of various experimental ulcers (e.g. NSAID, stress, ethanol) [55][56][57][58], as well as in H. pylori-associated ulcers [59]. It is well-established that excessive production of reactive oxygen species (ROS) and/or their decreased elimination by antioxidant enzymes induce cell and tissue damage by promoting lipid peroxidation and increasing the production of inflammatory mediators and proinflammatory cytokines [60].…”

“…Reduced mucosal antioxidative capacity and increased level of lipid peroxidation products (e.g. malondialdehyde) correlate well with macroscopic and histological mucosal damage, and agents endowed with antioxidant property are able to prevent ROS-mediated cellular damage [55][56][57][58]61]. Our results show that allyphenyline significantly increased the mucosal content of SOD (which enzyme catalyzes the dismutation of O2˙− into less noxius hydrogen peroxide (H2O2)) and CAT (which accelerates the breakdown of H2O2 to water and oxygen) compared to the ethanol-treated group, suggesting that the gastroprotective action of allyphenyline -at least partly -relies on its ability to enhance the activity of mucosal antioxidant enzymes and reduce the damaging effect of ROS.…”