Abstract OBJECTIVE: To investigate the relationship between apoptosis-related proteins in gastric mucosa, p53 and Bax, and Helicobacter pylori (H. pylori) infection in children. METHODS: p53 and Bax expression in gastric mucosa were measured using immunohistochemical technique in 33 children with gastric mucosal lesions. Presence/absence of H. pylori infection was detected by the rapid urease and pathological tests. RESULTS: Fifteen children (88%) showed positive expression of p53 in 17 children who were confirmed with H. pylori infection, compared with 9 (56%) in 16 H. pylori negative children. Thirteen children (76%) showed positive expression of Bax in the 17 children with H. pylori infection, compared with 6 (38%) in the 16 H. pylori negative children. The expression levels of p53 and Bax in the H. pylori positive group were significantly higher than those in the H. pylori negative group (P<0.05). CONCLUSIONS: H. pylori infection is associated with the over-expression of p53 and Bax proteins in gastric mucosa in children.［Chin J Contemp Pediatr, 2010, 12 (2):110-112］
LIU Wei-Ping,SUN Su-Fang,ZHANG Gui-Li. Expression of apoptosis-related proteins in gastric mucosa of children with Helicobacter pylori infection[J]. 中国当代儿科杂志, 2010, 12(2): 110-112.
LIU Wei-Ping,SUN Su-Fang,ZHANG Gui-Li. Expression of apoptosis-related proteins in gastric mucosa of children with Helicobacter pylori infection[J]. CJCP, 2010, 12(2): 110-112.
［1］Uemura N, Okamoto S, Yamamoto S, Matsumura N, Yamaguchi S, Yamakido M, et al. Helicobacter pylori infection and development of gastric cancer［J］. N Engl J Med, 2001, 345(11):784-789.
［2］Drumm B, Shermann P, Cutz E, Karmali M. Association of Campylobacter pylori on the gastric mucosa with antral gastritis in children ［J］. N Engl J Med, 1987, 316(25):1557-1561.
［3］Kato S, Nishino Y, Ozawa K, Konno M, Maisawa S, Toyoda S, et al. The prevalance of Helicobacter pylori in Japanese children with gastritis or peptic ulcer disease［J］. J Gastroenterol, 2004, 39(8):734-738.
［4］Blaser MJ. Hypotheses on the pathogenesis and natural history of Helicobacter pylori-induced inflammation ［J］. Gastroenterology, 1992, 102(2):720-727.
［5］Ozawa K, Kato S, Sekine H, Koike T, Minoura T, Iinuma K, et al. Gastric epithelial cell turnover and mucosal protection in Japanese children with Helicobacter pylori infection［J］. J Gastroenterol, 2005, 40(3):236-246.
［6］Sun Y. p53 and its downstream proteins as molecular targets of cancer［J］. Mol Carcinog, 2006, 45(6):409-415.
［7］Adams JM, Cory S. Bcl-2-regulated apoptosis: mechanism and therapeutic potential［J］. Curr Opin Immunol, 2007, 19(5):488-496.
［8］Sinicrope FA, Ruan SB, Cleary KR, Stephens LC, Lee JJ, Levin B. bcl-2 and p53 oncoprotein expression during colorectal tumorigenesis ［J］. Cancer Res, 1995, 55(2):237-241.
［9］Hoshi T, Sasano H, Kato K, Ohara S, Shimosegawa T, Toyota T, et al. Cell damage and proliferation in human gastric mucosa infected by Helicobacter pylori: a comparison before and after H. pylori eradication in nonatrophic gastritis［J］. Hum Pathol, 1999, 30(12):1412-1417.
［10］Rodier F, Campisi J, Bhaumik D.Two faces of p53: aging and tumor suppression［J］.Nucleic Acids Res, 2007, 35(22):7475-7484.
［12］Baik SC, Youn HS, Chung MH, Lee WK, Cho MJ, Ko GH, et al. Increased oxidative DNA damage in Helicobacter pylori-infected human gastric mucosa［J］. Cancer Res, 1996, 56(6):1279-1282.
［13］Adams JM, Cory S. The Bcl-2 apoptotic switch in cancer development and therapy［J］. Oncogene, 2007, 26(9):1324-1337.
［14］Liu HF, Liu WW, Wang GA, Teng XC. Effect of Helicobacter pylori infection on Bax protein expression in patients with gastric precancerous lesions［J］. World J Gastroenterol, 2005, 11(37):5899-5901.
