细胞增殖与凋亡在十二指肠胃反流患者胃黏膜病变进展中的变化

目的探讨细胞增殖与凋亡在原发性十二指肠胃反流（DGR）患者胃黏膜病变的发生发展中的作用。方法对58例原发性病理性DGR患者进行24h胃内胆汁监测，并行胃镜检查及胃黏膜活检，采用免疫组化方法分析不同病变胃黏膜组织Ki-67、Bcl-2蛋白的表达，采用TUNEL技术观察胃黏膜细胞凋亡情况。结果1．原发性病理性DGR患者胃黏膜上皮细胞增殖指数（PI）和凋亡指数（AI）均显著高于正常对照组（P〈0．05），高反流组PI、AI均高于低反流组（P〈0．05）；2．高反流组胃窦部萎缩性胃炎的检出率高于低反流组（P〈0．05）；3．在正常胃黏膜→浅表性胃炎→萎缩性胃炎→肠上皮化生发展过程中，PI、AI均逐渐升高且呈一致性升高。在发生异型增生时PI仍显著增加而AI显著下降。4．呈异型增生的患者胃黏膜上皮细胞Ki-67表达阳性率显著升高（P〈0．05），呈异型增生的患者胃黏膜上皮细胞Bcl-2阳性率高于其它各组（P〈0．05）。结论细胞增殖与凋亡失调可能在十二指肠反流液造成胃黏膜病变的进展中发挥重要作用，Ki-67、Bcl-2蛋白表达异常可能是DGR患者胃黏膜损伤及癌变的分子机制之一。

Cell proliferation and apoptosis of gastric mucosa in patients with duodena-gastric reflux

Objective To investigate the effects of cell proliferation and apoptasis on the develop-ment of gastric mucosal lesion in patients with primary pathological duodena-gastric reflux (DGR). Methods Gastroscopy, histologie examination of gastric mucosal biopsy and 24-hour intra-gastric bilirubin monitoring with Bilitec 2000 were performed in 58 patients with primary pathological DGR. Immunohisto-chemical staining was used to detect the expressions of Ki-67 and Bcl-2 proteins. Cell apoptosis in gastric mucesa was determined by TUNEL technique. Results The proliferating index (PI) and apoptosis index (AI) in patients with primary pathological DGR were significantly higher than those in control group (P< 0.05). The differences of PI and AI between high reflux group and low reflux group were significant (P< 0.05). The incidence difference of chronic superficial gastritis (CSG) and chronic atrophic gastritis (CAG) in gastric antrum between the two groups was significant (P<0.05). With lesion progressing from normal gastric mucosa, CSG, CAG to intestinal metaplasia (IM), PI and AI increased gradually and consistently. PI was still on the rise after dysplasia (Dys), but AI decreased. The positive expression rate of Ki-67 in Dys were significantly higher than that of other groups (P<0.05), so was that of Bcl-2 (P<0.05). Conclusion Cell proliferation and apoptesis may be one aspect of the main pathogenesis of gastric mucesa lesion and cell dysplasia in patients with primary pathological DGR. Over-expreasion of Ki-67 and Bcl-2 proteins in CAG, IM and Dys may play a key role in the development of gastric cancer.