Han Wei, Wang Zhen-jun, Zhao Bo, Yang Xin-qing, Wang Dong, Wang Jian-pin, Tang Xiu-ying, Zhao Fa, Hung Yan-ting
Department of General Surgery, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Zhonghua Wei Chang Wai Ke Za Zhi. 2005 Jan;8(1):56-9.
To investigate the pathological variations in internal hemorrhoid and evaluate the expression of nitric- oxide synthase(NOS),vascular endothelial growth factor(VEGF),matrix metalloproteinase- 2(MMP2) and MMP9.
Normal anal cushion and internal hemorrhoids tissue samples were obtained from 24 patients with iii degree hemorrhoids after procedure for prolapse and hemorrhoids(PPH) procedure. The expression of NOS, VEGF, MMP2, MMP9 and CD34 were detected by immunohistochemical staining; the microvessel density (MVD) was counted by anti- CD34 antibody; the elastic fibers were detected by orcein staining.
There were statistically significant differences in the expression of MVD, VEGF, MMP9 between internal hemorrhoid tissue and normal anal cushions(P< 0.05). iNOS was significantly increased in hemorrhoid tissue, but no significant difference between normal anal cushions and hemorrhoid tissue. Morphological abnormalities such as breaking, distortion, mortality, hyaline degeneration were found in elastic fibers of internal hemorrhoid tissue, but not in normal anal cushions.
Angiogenesis is evident in hemorrhoid tissue, suggesting the possible mechanism in the pathogenesis of hemorrhoids. The direct degeneration effect of MMP9 on supporting structure elastic fibers in anal cushion is another important mechanism. The high expression of iNOS suggests the inflammatory factors involve in the pathogenesis of hemorrhoids, and NO may be involve in pathological effect on hemorrhoids.
研究内痔的病理变化,并评估一氧化氮合酶(NOS)、血管内皮生长因子(VEGF)、基质金属蛋白酶-2(MMP2)和MMP9的表达。
从24例Ⅲ度痔患者行吻合器痔上黏膜环切术(PPH)后获取正常肛垫和内痔组织样本。采用免疫组织化学染色检测NOS、VEGF、MMP2、MMP9和CD34的表达;用抗CD34抗体计数微血管密度(MVD);用orcein染色检测弹性纤维。
内痔组织与正常肛垫在MVD、VEGF、MMP9表达上有统计学差异(P<0.05)。痔组织中诱导型一氧化氮合酶(iNOS)显著升高,但正常肛垫与痔组织之间无显著差异。内痔组织弹性纤维出现断裂、扭曲、死亡、玻璃样变性等形态学异常,而正常肛垫未出现。
痔组织中血管生成明显,提示可能是痔发病机制。MMP9对肛垫支撑结构弹性纤维的直接降解作用是另一个重要机制。iNOS的高表达提示炎症因子参与痔的发病机制,且NO可能参与痔的病理作用。