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目的探讨溃疡性结肠炎(UC)患者大肠黏膜组织中凋亡蛋白半乳糖凝集素3(Gal-3)与B淋巴细胞瘤-2基因(Bcl-2)的表达及意义。方法应用免疫组织化学SP法检测UC患者60例(UC组)和正常对照者20例(对照组)大肠黏膜组织中的Gal-3与Bcl-2的表达,并分析UC大肠黏膜组织中Gal-3与Bcl-2表达的关系。以细胞质或细胞核中出现明显的棕黄色颗粒为阳性细胞,根据染色强度及阳性细胞数进行光镜下半定量分析。结果 Gal-3与Bcl-2的表达均在上皮细胞的细胞质,Gal-3在正常大肠黏膜上皮细胞中呈强阳性表达,在UC大肠上皮细胞的表达明显减弱,且与肠镜下病变程度相关;Bcl-2在正常大肠黏膜上皮细胞中呈弱表达,在UC大肠黏膜上皮细胞的表达明显增强,主要为固有层炎性细胞表达增强,与肠镜下病变程度无明显关系。Gal-3与Bcl-2的表达与患者的年龄、性别、病程均无明显相关。Pearson相关分析显示Gal-3与Bcl-2的阳性表达程度不具有关联性。结论 Gal-3与Bcl-2蛋白在UC的发生和发展中起重要作用,可望成为UC早期诊断和预后判断的指标,两者在UC的发病中可能独立起作用。
Objective To investigate the expression of Bcl-2 and Bcl-2 in colorectal mucosa of patients with ulcerative colitis (UC). Methods Immunohistochemical SP method was used to detect the expression of Gal-3 and Bcl-2 in colorectal mucosa of 60 patients with UC (UC group) and 20 normal controls (control group), and to analyze the expression of Gal- 3 and Bcl-2 expression. With the obvious cytoplasm or nucleus in the brown granules as positive cells, according to the staining intensity and the number of positive cells semi-quantitative analysis by light microscopy. Results The expression of Gal-3 and Bcl-2 were all in the cytoplasm of epithelial cells. The expression of Gal-3 in normal colorectal mucosa epithelial cells was strongly positive, and was significantly decreased in UC colorectal epithelial cells Bcl-2 was weakly expressed in normal colorectal mucosa epithelial cells. The expression of Bcl-2 was significantly increased in UC colorectal epithelial cells. The expression of Bcl-2 was mainly increased in inflammatory cells of lamina propria, which was not related to the degree of lesion under colonoscopy. There was no significant correlation between the expression of Gal-3 and Bcl-2 in patients with age, gender and course of disease. Pearson correlation analysis showed that the positive expression of Gal-3 and Bcl-2 had no correlation. Conclusions Gal-3 and Bcl-2 proteins play an important role in the pathogenesis and development of UC, which may be an indicator of early diagnosis and prognosis of UC. Both of them may play an independent role in the pathogenesis of UC.