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AIM:To investigate the effect of Helicobacter pylori (Hpylori)infection on the expressions of Bcl-2 family members ingastric adenocarcinoma.METHODS:Gastric adenocarcinoma and resection margintissues of 95 patients were studied.Semi-quantitative RT-PCRwas used to measure Bid,Bax and Bcl-2 mRNA expressions.RESULTS:Expressions of Bid and Bax in gastric adenocarcinomatissues without H pylori infection,with cagA~- H pylori infectionand cagA~+ H pylori infection increased significantly in turn(Bid,0.304,0.422 and 0.855 respectively,P<0.05; Bax,0.309,0.650 and 0.979 respectively,P<0.05).Bcl-2 mRNAlevels increased significantly in gastric adenocarcinomatissues with cagA~- Hpylori infection and cagA~+ Hpyloriinfection,compared with those without Hpylori infection(0.696 and 0.849 vs 0.411,P<0.05).Expressions of Bid,Bax and Bcl-2 in resection margin tissues without Hpyloriinfection,with cagA~- H pylori infection and cagA~+ H pyloriinfection increased significantly in turn (Bid,0.377,0.686and 0.939 respectively,P<0.05; Bax,0.353,0.645 and1.001 respectively,P<0.05; Bcl-2,0.371,0.487 and 0.619respectively,P<0.05).In H pylori negative specimens,expressions of Bid and Bax correlated negatively with thatof Bcl-2 respectively in adenocarcinoma tissues (Bid vs Bcl-2,r=-0.409,P<0.05; Bax vs Bcl-2,r=-0.451,P<0.05).InH pylori positive specimens,expressions of Bid and Bax didnot correlate with that of Bcl-2 in adenocarcinoma tissues(Bid vsBcl-2,r=-0.187,P>0.05; Bax vs Bcl-2,r=0.201,P>0.05),but correlated positively with that of Bcl-2 respectivelyin resection margin tissues (Bid vs Bcl-2,r=0.331,P<0.05;Bax vs Bcl-2,r=-0.295,P<0.05).CONCLUSION:H pylori may enhance Bid,Bax and Bcl-2mRNA levels and cause deregulation of these apoptosis-associated genes expressions,which may play a role duringdevelopment of gastric adenocarcinoma induced by H pylori.
AIM: To investigate the effect of Helicobacter pylori (Hpylori) infection on the expressions of Bcl-2 family members ingastric adenocarcinoma. METHODS: Gastric adenocarcinoma and resection margins of patients were studied. Semi-quantitative RT-PCR was used to measure Bid, Bax and Bcl-2 mRNA expressions .RESULTS: Expressions of Bid and Bax in gastric adenocarcinomatissues without H pylori infection, with cagA ~ -H pylori infection and cagA ~ + H pylori infection increased significantly in turn (Bid, 0.304, 0.422 and 0.855 respectively, P <0.05; Bax, 0.309, 0.650 and 0.979 respectively, P <0.05) .Bcl-2 mRNAlevels increased significantly in gastric adenocarcinomatissues with cagA ~ -Hpylori infection and cagA ~ + Hpyloriinfection, compared with those without Hpylori infection (0.696 and 0.849 vs 0.411 , P <0.05) .Expressions of Bid, Bax and Bcl-2 in resecting margin tissues without Hpylori infection, with cagA ~ -H pylori infection and cagA ~ + H pylori infection increased significantly in turn (Bid, 0.377,0.686 and 0.93 P <0.05) .In H pylori negative specimens, expressions of Bid and Bax correlated negatively (P <0.05), P <0.05, Bax, 0.353, 0.645 and1.001 respectively, P < with that of Bcl-2 in adenocarcinoma tissues respectively (P <0.05 vs. Bcl-2, r = -0.409, P < Bax didnot correlate with that of Bcl-2 in adenocarcinoma tissues (Bid vs Bcl-2, r = -0.187, P> 0.05; Bax vs Bcl- CONCLUSION: H pylori may enhance Bid, Bax and Bcl-2 mRNA levels (Bax vs Bcl-2, r = -0.295, P < and cause deregulation of these apoptosis-associated genes expressions, which may play a role during development of gastric adenocarcinoma induced by H pylori.