目的:观察大鼠胃粘膜在幽门螺杆菌(Hp)培养滤液长期作用下的组织学变化及其对大鼠实验性胃癌的促癌作用。方法:分别以0.25%和0.5%的Hp培养滤液让大鼠自由饮用，观察不同时间大鼠胃粘膜厚度、表面粘液含量、DNA合成速率及组织学变化；并观察不同时相应用Hp培养滤液对甲基硝基亚硝基胍(MNNG)诱癌的促癌作用。结果:实验第5周时，实验组大鼠胃粘膜厚度明显变薄，表面粘液含量减少和DNA合成速率加快，随实验时间的延长，上述改变进一步加重。至52周实验结束时，0.5% Hp培养滤液组大鼠腺胃粘膜肠化生、硫酸粘液阳性肠化生和异型增生的发生率(57%、39%、18%)明显高于0.25% Hp培养滤液组(28%、10%、3%)和正常对照组(7%、0%、0%)。无论在给予MNNG以前、同时或以后饮用Hp培养滤液，大鼠胃癌和癌前病变的发生率均明显增加。结论:Hp的毒性产物可能具有直接的诱癌和促癌作用。

Objective To investigate the effects of cell-matrix adhesion on drug resistance of tumor cells. Methods MTT test was conducted to study the effects of adhesion between A549-ADR tumor cells and fibronection on sensitivity to anti-cancer drugs, the expression of bcl-2 and Bax gene protein was analyzed by flow cytometry. Results The extent of drug resistance decreased to control levels after the binding was blocked by using anti-β1 integrin antibody. The expression of bcl-2 protein was increased and the Bax protein was decreased when the tumor cell binds to fibronectin, the rate of apoptosis was also significantly decreased when the tumor cell binds to fibronectin and increased after blocked by antiβ-1 integrin antibody. Conclusion Adhesion of tumor cells with fibronectin can increase drug resistance of tumor cells probably by regulating the expression of apoptosis-related genes and the rate of apoptosis.