Application research of Galectin-3 and Bcl-2 in colorectal tissues of patients with ulcerative colitis
10.3969/j.issn.1671-8348.2015.02.012
- VernacularTitle:半乳糖凝集素3与Bcl-2在溃疡性结肠炎患者大肠黏膜中的应用研究
- Author:
Qifang ZHANG
;
Xiaoyan LI
;
Yuanyuan WANG
;
Xirong LI
;
Zhuolin CHEN
;
Yi ZHENG
;
Siming HE
;
Yongchang CHEN
;
Haixing JIANG
- Publication Type:Journal Article
- Keywords:
colitis,ulcerative;
Galectin-3;
immunohistochemistry;
Bcl-2
- From:
Chongqing Medicine
2015;(2):180-182,185
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the expressions and significance of Galectin‐3 and Bcl‐2 in colorectal tissues of patients with ulcerative colitis(UC) .Methods Immunohistochemical SP method was applied to detected the expression of Galectin‐3 and Bcl‐2 in colorectal tissues of 60 patients in UC group and 20 healthy adults in the control group ,and analyzed the relationship of the expres‐sions between Galectin‐3 and Bcl‐2 .It was regarded as positive cell when obvious dark brown granules appeared in cytoplasm or cyteblast .Semi‐quantitative analysis was used basing on the staining intensity and the amount of the staining intensity and positive cells .Results Galectin‐3 and Bcl‐2 proteins expressed in cytoplasm .Galectin‐3 showed strong expression in normal colorectal epi‐thelium but weak in UC inflammatory tissues ,and it was associated with different lesion degrees under endoscopy .The expressions of Bcl‐2 were weak in normal colorectal epithelium ,and it enhanced significantly in UC inflammatory tissues ,especially in inflamma‐tory cells of laminae propria ,and it was not associated with different lesion degrees under endoscopy .The expression of Galectin‐3 and Bcl‐2 was not associated with the age ,sex of patients and the course of UC .Pearson correlation analysis showed that the posi‐tive expressions of Galectin‐3 and Bcl‐2 had no relevance .Conclusion Galectin‐3 and Bcl‐2 involved in the pathogenesis of UC . They may be able to used as markers of early diagnosis and prognosis in UC and may play the role in the pathogenesis of UC inde‐pendently .
