Objective: To compare the expression of group D A secretory phospholipase A2 (II A sPLA2 ) between gastric card-noma and noncancerous tissues and to analyze the correlations of U A sPLA2 expression with helicobacter pylori ( Hp) injection, mi-crovessel formation, and chnicopathologic characteristics. Methods: One hundred pathologic specimens from patients with advanced gastric carcinoma ( AGC ) were collected. The MaxVision immunohistochemical method was used to measure the expression of D A sP-LA2 protein in the 100 AGC cases, in addition to 30 cases with normal gastric mucosa (NGM), 30 with chronic inflammation plus intestinal metaplasia ( IM ), and 30 with dysplasia ( DYS ). In addition, the Hp infection rate and CD34-labeled microvessel density were determined. Results: Expression of D A sPLA2 ( positive status ) was significantly higher in the IM group ( 88.3% ), the DYS group ( 66.7% ), and the AGC group ( 44.0 % ) than in the NGM group ( 23.3% ) ( P< 0.05 ). However, the expression of D A sPLA2 was significantly lower in the AGC group than in the IM and DYS groups (P<0.05 ). There were no significant differences in the rate of Hp infection among the three groups ( IM: 43.3%, DYS: 36.7%, AGC: 38.0%; P>0.05 ) but Hp infection rate was significantly higher in all these groups than in the NGM group ( 13.3%) (P<0.05 ). In the IM and DYS groups, the expression of 11A sPLA2 was higher in the specimens with Hp infection than in those without Hp infection ( P < 0.05 ). In the AGC group, however, there were no statistical differences in D A sPLA2 expression between specimens with and without Hp infection ( P > 0.05 ). Positive expression of D A sPLA2 was correlated with the infiltration depth of AGC and nodal metastasis (P< 0.05 ). In the AGC group, the microvessel density was significantly lower in the specimens with higher D A sPLA2 expression ( P < 0.05 ). Conclusion: Group D A sPLA2 may participate in the pathogenesis and development of gastric carcinoma. The loss of D A sPLA2 expression may be an early pathogenic event in gastricmor immune response in vivo. Moreover, the loss of IIA sPLA2 expression may contribute to the invasion, metastasis, and microvessel formation of gastric carcinoma.%目的:分析ⅡA分泌型磷脂酶A2(ⅡA sPLA2)在胃癌及非癌组织中的表达,探讨ⅡA sPLA2表达与幽门螺杆菌感染(Hp)、微血管生成和胃癌临床病理特征间的相关性.方法:采用MaxVision免疫组化法检测100例进展期胃癌组织(AGC)、30例基本正常胃黏膜(NGM)、30例慢性炎症伴肠化(IM)、30例不典型增生(DYS)组织中的ⅡA sPLA2蛋白的表达情况、Hp的感染率以及CD34标记的微血管密度.结果:ⅡA sPLA2在IM、DYS及AGC中的阳性检出率分别为88.3%、66.7%及44.0%,显著高于阳性检出率为23.3%的NGM(P<0.05),但ⅡA sPLA2在AGC中的表达水平明显低于IM及DYS(P<0.05).IM、DYS、AGC组的Hp感染率分别为43.3%、36.7%及38.0%,差异无统计学意义(P>0.05),且均高于NGM组的为13.3%Hp感染率(P<0.05).IM及DYS组中,Hp阳性感染的组织标本的ⅡA sPLA2表达水平明显高于Hp阴性的组织标本(P<0.05),而在AGC组,Hp阳性感染与Hp阴性的标本中ⅡA sPLA2的表达差异无统计学意义(P>0.05).ⅡA sPLA2的表达水平与AGC的浸润深度、淋巴结转移有关(P<0.05),ⅡAsPLA2高表达的AGC标本间质微血管密度明显低于ⅡA sPLA2低表达的AGC标本(P<0.05).结论:ⅡA sPLA2参与了胃癌的发生与演化,其表达下调可能是胃癌形成的早期事件,且与Hp感染无关.ⅡA sPLA2表达水平下调可能是胃癌抗肿瘤免疫失调的一个重要环节.ⅡA sPLA2表达下调可能对胃癌的侵袭、转移以及肿瘤微血管生成存在一定的影响.
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