Preventive Effect of Actinidia Valvata Dunn Extract on N-methyl-N'-nitro-N-nitrosoguanidine-induced Gastrointestinal Cancer in Rats

Abstract

Asian Pac J Cancer Prev, 15 (15), [6363][6364][6365][6366][6367] Introduction Gastric cancer remains a major global problem. In 2008, 989,600 new stomach cancer cases and 738,000 deaths occurred, accounting for 8% of the total cases and 10% of total deaths, respectively (Jemal et al., 2011). Notwithstanding the global declining incidence of gastric cancer, mortality is continuously rising in Asian countries (Hu et al., 2004). Surgery is considered as the gold standard for localized gastric cancer, but most cases are diagnosed at an advanced stage. The five-year survival rate of patients with advanced gastric cancer for surgical treatment is less than 40% (Rasul et al., 2012). Recent primary prevention strategies for gastric cancer focus on behavior modification, including the eradication of Helicobacter pylori, reduction of salt intake, increase in food containing protective factors (fruit,vegetables, soybean products, non-fermented soy-foods,whole-grain) and vitamin C consumption, abolition of smoking, and chemoprevention (Tsugane et al., 2004 AbstractPurpose: This study was conducted to assess the preventive effect of Actinidia valvata Dunn (AVD) extract on an animal model of gastrointestinal carcinogenesis on the basis of changes in tumor incidence, cell proliferation, and apoptosis. Materials and Methods: Seventy-five male Wistar rats were divided into five different treatment groups with 15 rats in each group. Group I was given normal feed, whereas Groups II to IV were treated with 10% sodium chloride in the first six weeks and 100ug/mL of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in drinking water for 24 weeks. Group II was then given normal feed, whereas Group III was given AVD extract (0.24g/kg/day) for 12 weeks. Group IV was given AVD extract from the first week to the 36 th week, whereas Group V was treated with AVD extract alone for 36 weeks. All rats were sacrificed at the end of the 36-week experiment and assessed for the presence of gastrointestinal tumors. The occurrence of cancer was evaluated by histology. Bax, Bcl-2, Caspase-3, and cyclinD1 were determined by immunohistochemical staining and Western blotting. Results: The incidences of gastric cancer were 0% in Group I, 73.3% in Group II, 33.3% in Group III, 26.7% in Group IV, and 0% in Group V. Bcl-2 and cyclinD1 expression was decreased in AVD extract treated groups, whereas Bax and Caspase-3 expression was increased. Comparison with group II revealed significant differences (p<0.01). Conclusions: AVD extract exhibits an obvious preventive effect on gastrointestinal carcinogenesis induced by MNNG in rats through the regulation of cell proliferation and apoptosis.

miR-374 mediates the malignant transformation of gastric cancer-associated mesenchymal stem cells in an experimental rat model

“…Among all the established animal models of gastric cancer (6–8), the rat model induced with chemical carcinogens such as N -methyl- N '-nitro- N -nitrosoguanidine (MNNG) is widely used due to the simple operation, cheap cost, easy keep and lower natural cancer rate (9). It has been shown that MNNG treatment results in the mutation of DNA and increased oxidative injury, which is critical to gastric carcinogenesis (10,11).…”

Effect of ethyl acetate extract of usnea longissima on esophagogastric adenocarcinoma in rats

“…The review of the literature shows that MNNG is used in different doses and for different durations to develop a cancer model. For example, Wang et al 18 reported that they induced gastrointestinal cancer in rats mixing MNNG with their drinking water for 24 weeks. In an earlier study, we used a similar dose of MNNG over a similar period to induce cancer in rats 15 .…”

Clinical significance of the phosphorylation of MAPK and protein expression of cyclin D1 in human osteosarcoma tissues

“…Studies have indicated that the overexpression of cyclin D1 may result in a reduction of the G1 phase of the cell cycle (15)(16)(17), leading to progression into the S phase and completing the duplication of DNA. The increase in the protein expression of cyclin D1 is observed in certain primary malignant tumors, including parathyroid adenoma, neck squamous-cell carcinoma, breast cancer, esophageal cancer, and hepatocellular carcinoma (18)(19)(20)(21). As MAPK is expressed as an upstream gene of cyclin D1, the increase in the level of p-MAPK in osteosarcoma was directly proportional to the intensity of cyclin D1-positive staining.…”