The action mechanism of matrix metalloproteinases-2 （MMP-2） and tissue inhibitor of metalloproteinases-2 （TIMP-2） in the genesis, development and degeneration of haemangioma was investigated by detecting their exp...The action mechanism of matrix metalloproteinases-2 （MMP-2） and tissue inhibitor of metalloproteinases-2 （TIMP-2） in the genesis, development and degeneration of haemangioma was investigated by detecting their expression in the tissue of haemangioma in different phases by using the immunohistochemistry. Fifty paraffin-embedded specimens of skin capillary haemangioma were collected, which were documented in the Department of Pathology, Renmin Hospital of Wuhan University from 2000 to 2006. All samples were stained by regular HE method, and proliferative cell nuclear antigen （PCNA） was tested by immunohistochemical S-P method. The samples were classified according to the Mulliken criteria and the expression pattern of PCNA. Immunohistochemical S-P method was ap- plied to detect the expression of MMP-2 and TIMP-2 in proliferative and degenerative phases of cutaneous capillary haemangioma, and in normal skin tissues. In combination with the detection of the expression of factor Ⅷ-related antigen, it was verified that in haemangioma tissues, the cells expressing MMP-2 and TIMP-2 were vascular endothelial cells. The MMP-2 and TIMP-2 expression was quantitatively analyzed by image analysis system （HPIAS-1000）, and one-way ANOVA（107） and SNK（q） test were done to analyze average absorbance （A） and positive area rate of immunohistochemically positive particles by using SPSS11.5. The results showed： （1） Among 50 samples of haemangioma, there were 26 proliferative haemangiomas, and 24 degenerative haemangiomas, respectively; （2） The expression of MMP-2 was weak in normal vascular endothelial cells, cytoplasm of connective tissues and extracellular matrix around blood vessels. The expression of MMP-2 in proliferative group was significantly higher than in degenerative group and control group （normal skin） （P〈0.05）, but there was no statistically significant difference between the latter two groups; （3） TIMP-2 was highly expressed in normal tissues, degenerative vascular endothelial cells, cytoplasm of connective tissues and extracellular matrix around blood vessels. The expression level of TIMP-2 in proliferative phase was significantly lower than in degenerative phase （P〈0.05）, and the expression of TIMP-2 in proliferative phase was significantly different from that in degenerative phase and normal tissues （P〈0.05）. It was concluded that in proliferative phase of haemangioma, MMP-2 may promote over-proliferation of endothelial cells of haemangioma, and in degenerative phase, TIMP-2 can inhibit the proliferation of endothelial cells of haemangioma. The two substances play important roles in the genesis, development and degeneration of haemangiomas.展开更多
目的探讨自然分娩初产妇血清基质金属蛋白酶组织抑制因子-1(tissue inhibitor of metall oproteinase-1,TIMP-1)、血管内皮生长因子(vascular endothelial growth factor,VEGF)水平对产后压力性尿失禁(post partum stress urinary incon...目的探讨自然分娩初产妇血清基质金属蛋白酶组织抑制因子-1(tissue inhibitor of metall oproteinase-1,TIMP-1)、血管内皮生长因子(vascular endothelial growth factor,VEGF)水平对产后压力性尿失禁(post partum stress urinary incontinence,PSUI)严重程度的预测价值。方法选取2019年12月至2023年7月220例PSUI自然分娩初产妇为病例组,根据尿垫试验结果分为轻度组158例和中重度组62例。另纳入同期220例无PSUI的自然分娩初产妇作为对照组。采用ELISA法检测入组者血清TIMP-1、VEGF水平;采用Pearson法分析PSUI患者血清TIMP-1与VEGF的相关性;采用多因素Logistic回归分析PSUI患者疾病严重程度的影响因素;采用受试者工作特征曲线分析血清TIMP-1、VEGF对PSUI患者疾病严重程度的预测价值。结果病例组血清TIMP-1水平显著低于对照组,血清VEGF水平显著高于对照组(P<0.01)。中重度组血清TIMP-1水平显著低于轻度组,血清VEGF水平、年龄≥35岁比例、新生儿体质量显著高于轻度组(P<0.05,P<0.01)。PSUI患者血清TIMP-1与VEGF呈负相关(r=-0.671,P<0.05)。TIMP-1是PSUI患者疾病程度加重的保护因素(P<0.01),VEGF是PSUI患者疾病程度加重的危险因素(P<0.01)。TIMP-1、VEGF单独及联合预测PSUI患者疾病严重程度的曲线下面积(area under curve,AUC)分别为0.857、0.808、0.901,其中联合预测的AUC高于二者单独预测(P<0.01)。结论PSUI患者血清TIMP-1低表达,VEGF高表达,且TIMP-1、VEGF与病情程度密切相关,二者联合在预测PSUI患者疾病严重程度方面有较高的价值。展开更多
目的探讨基质金属蛋白酶(matrix metalloproteinase,MMP)-2、14及基质金属蛋白酶组织抑制因子-2(tissueinhibitor of metalloproteinase,TIMP-2)在胃癌中的表达及其意义。方法用免疫组织化学方法(SP法)检测80例胃癌手术患者胃癌组织及3...目的探讨基质金属蛋白酶(matrix metalloproteinase,MMP)-2、14及基质金属蛋白酶组织抑制因子-2(tissueinhibitor of metalloproteinase,TIMP-2)在胃癌中的表达及其意义。方法用免疫组织化学方法(SP法)检测80例胃癌手术患者胃癌组织及30例同期癌旁≥5cm正常组织中MMP-2、MMP-14及TIMP-2的表达。结果①在胃癌、正常胃组织中,MMP-2阳性表达率分别为75.00%和36.67%,MMP-14阳性表达率分别为82.50%和33.33%,差异有统计学意义(均P<0.01);TIMP-2阳性表达率分别为45.00%和40.00%,差异无统计学意义。②癌组织中,MMP-2、MMP-14的表达与肿瘤分化程度、浸润深度、淋巴结有无转移和TNM临床分期密切相关(均P<0.01)。TIMP-2的表达仅与淋巴结有无转移相关(P<0.05)。③生存期<2年患者的MMP-2、MMP-14表达率明显高于生存期≥2年患者(均P<0.01)。结论胃癌组织中,MMP-2、MMP-14高表达,联合检测MMP-2、MMP-14或MMP-2、MMP-14、TIMP-2可作为胃癌恶性程度及预后判断的指标。展开更多
目的:观察丹酚酸B盐(salvianolic acid B,SA-B)对肝纤维化大鼠肝组织转化生长因子-β1 (TGF-β1)、基质金属蛋白酶-2(MMP-2)和基质金属蛋白酶组织抑制因子-2(TIMP-2)表达的影响,并探讨SA-B抗肝纤维化的可能机制.方法:♂SD大鼠30只随机...目的:观察丹酚酸B盐(salvianolic acid B,SA-B)对肝纤维化大鼠肝组织转化生长因子-β1 (TGF-β1)、基质金属蛋白酶-2(MMP-2)和基质金属蛋白酶组织抑制因子-2(TIMP-2)表达的影响,并探讨SA-B抗肝纤维化的可能机制.方法:♂SD大鼠30只随机分为正常对照组、模型组和丹酚酸B治疗组,以5 mL/L的二甲基亚硝胺(DMN)建立肝纤维化模型,治疗组在造模4 wk后给予SA-B治疗4 wk.应用HE,Masson染色观察肝组织病理纤维化分级,全自动生化分析仪检测ALT、AST和Alb,放免法检测HA和LN,S-P免疫组织化学方法检测TGF-β1、MMP-2和TIMP-2蛋白质的表达.结果:与模型组相比,SA-B能改善肝纤维化大鼠肝脏病理组织学结构,治疗组血清ALT、AST、HA和LN水平明显减低(87.0±28.7 U/L vs 190.4±27.4 U/L.85.6±25.3 U/L vs 178.2±15.9 U/L,179.7±32.8 mg/L vs 433.3±86.1 mg/L,135.6±21.1 mg/L vs 224.7±29.2 mg/L,均P<0.01),经SA-B干预后TGF-β1和TIMP-2表达明显下降,与模型组相比有显著性差异(18.53±2.54 vs 12.78±2.65,21.88±3.83 vs 14.69±4.51,均P<0.01),而MMP-2表达水平无明显变化.结论:SA-B能改善肝纤维化大鼠肝脏病理组织学结构,可能通过抑制TGF-β1和TIMP-2表达而促进肝纤维化的逆转.展开更多
基金supported by a grant from the National Natural Sciences Foundation of China (No.30872688)
文摘The action mechanism of matrix metalloproteinases-2 （MMP-2） and tissue inhibitor of metalloproteinases-2 （TIMP-2） in the genesis, development and degeneration of haemangioma was investigated by detecting their expression in the tissue of haemangioma in different phases by using the immunohistochemistry. Fifty paraffin-embedded specimens of skin capillary haemangioma were collected, which were documented in the Department of Pathology, Renmin Hospital of Wuhan University from 2000 to 2006. All samples were stained by regular HE method, and proliferative cell nuclear antigen （PCNA） was tested by immunohistochemical S-P method. The samples were classified according to the Mulliken criteria and the expression pattern of PCNA. Immunohistochemical S-P method was ap- plied to detect the expression of MMP-2 and TIMP-2 in proliferative and degenerative phases of cutaneous capillary haemangioma, and in normal skin tissues. In combination with the detection of the expression of factor Ⅷ-related antigen, it was verified that in haemangioma tissues, the cells expressing MMP-2 and TIMP-2 were vascular endothelial cells. The MMP-2 and TIMP-2 expression was quantitatively analyzed by image analysis system （HPIAS-1000）, and one-way ANOVA（107） and SNK（q） test were done to analyze average absorbance （A） and positive area rate of immunohistochemically positive particles by using SPSS11.5. The results showed： （1） Among 50 samples of haemangioma, there were 26 proliferative haemangiomas, and 24 degenerative haemangiomas, respectively; （2） The expression of MMP-2 was weak in normal vascular endothelial cells, cytoplasm of connective tissues and extracellular matrix around blood vessels. The expression of MMP-2 in proliferative group was significantly higher than in degenerative group and control group （normal skin） （P〈0.05）, but there was no statistically significant difference between the latter two groups; （3） TIMP-2 was highly expressed in normal tissues, degenerative vascular endothelial cells, cytoplasm of connective tissues and extracellular matrix around blood vessels. The expression level of TIMP-2 in proliferative phase was significantly lower than in degenerative phase （P〈0.05）, and the expression of TIMP-2 in proliferative phase was significantly different from that in degenerative phase and normal tissues （P〈0.05）. It was concluded that in proliferative phase of haemangioma, MMP-2 may promote over-proliferation of endothelial cells of haemangioma, and in degenerative phase, TIMP-2 can inhibit the proliferation of endothelial cells of haemangioma. The two substances play important roles in the genesis, development and degeneration of haemangiomas.
文摘目的探讨自然分娩初产妇血清基质金属蛋白酶组织抑制因子-1(tissue inhibitor of metall oproteinase-1,TIMP-1)、血管内皮生长因子(vascular endothelial growth factor,VEGF)水平对产后压力性尿失禁(post partum stress urinary incontinence,PSUI)严重程度的预测价值。方法选取2019年12月至2023年7月220例PSUI自然分娩初产妇为病例组,根据尿垫试验结果分为轻度组158例和中重度组62例。另纳入同期220例无PSUI的自然分娩初产妇作为对照组。采用ELISA法检测入组者血清TIMP-1、VEGF水平;采用Pearson法分析PSUI患者血清TIMP-1与VEGF的相关性;采用多因素Logistic回归分析PSUI患者疾病严重程度的影响因素;采用受试者工作特征曲线分析血清TIMP-1、VEGF对PSUI患者疾病严重程度的预测价值。结果病例组血清TIMP-1水平显著低于对照组,血清VEGF水平显著高于对照组(P<0.01)。中重度组血清TIMP-1水平显著低于轻度组,血清VEGF水平、年龄≥35岁比例、新生儿体质量显著高于轻度组(P<0.05,P<0.01)。PSUI患者血清TIMP-1与VEGF呈负相关(r=-0.671,P<0.05)。TIMP-1是PSUI患者疾病程度加重的保护因素(P<0.01),VEGF是PSUI患者疾病程度加重的危险因素(P<0.01)。TIMP-1、VEGF单独及联合预测PSUI患者疾病严重程度的曲线下面积(area under curve,AUC)分别为0.857、0.808、0.901,其中联合预测的AUC高于二者单独预测(P<0.01)。结论PSUI患者血清TIMP-1低表达,VEGF高表达,且TIMP-1、VEGF与病情程度密切相关,二者联合在预测PSUI患者疾病严重程度方面有较高的价值。
文摘目的探讨基质金属蛋白酶(matrix metalloproteinase,MMP)-2、14及基质金属蛋白酶组织抑制因子-2(tissueinhibitor of metalloproteinase,TIMP-2)在胃癌中的表达及其意义。方法用免疫组织化学方法(SP法)检测80例胃癌手术患者胃癌组织及30例同期癌旁≥5cm正常组织中MMP-2、MMP-14及TIMP-2的表达。结果①在胃癌、正常胃组织中,MMP-2阳性表达率分别为75.00%和36.67%,MMP-14阳性表达率分别为82.50%和33.33%,差异有统计学意义(均P<0.01);TIMP-2阳性表达率分别为45.00%和40.00%,差异无统计学意义。②癌组织中,MMP-2、MMP-14的表达与肿瘤分化程度、浸润深度、淋巴结有无转移和TNM临床分期密切相关(均P<0.01)。TIMP-2的表达仅与淋巴结有无转移相关(P<0.05)。③生存期<2年患者的MMP-2、MMP-14表达率明显高于生存期≥2年患者(均P<0.01)。结论胃癌组织中,MMP-2、MMP-14高表达,联合检测MMP-2、MMP-14或MMP-2、MMP-14、TIMP-2可作为胃癌恶性程度及预后判断的指标。
文摘目的:观察丹酚酸B盐(salvianolic acid B,SA-B)对肝纤维化大鼠肝组织转化生长因子-β1 (TGF-β1)、基质金属蛋白酶-2(MMP-2)和基质金属蛋白酶组织抑制因子-2(TIMP-2)表达的影响,并探讨SA-B抗肝纤维化的可能机制.方法:♂SD大鼠30只随机分为正常对照组、模型组和丹酚酸B治疗组,以5 mL/L的二甲基亚硝胺(DMN)建立肝纤维化模型,治疗组在造模4 wk后给予SA-B治疗4 wk.应用HE,Masson染色观察肝组织病理纤维化分级,全自动生化分析仪检测ALT、AST和Alb,放免法检测HA和LN,S-P免疫组织化学方法检测TGF-β1、MMP-2和TIMP-2蛋白质的表达.结果:与模型组相比,SA-B能改善肝纤维化大鼠肝脏病理组织学结构,治疗组血清ALT、AST、HA和LN水平明显减低(87.0±28.7 U/L vs 190.4±27.4 U/L.85.6±25.3 U/L vs 178.2±15.9 U/L,179.7±32.8 mg/L vs 433.3±86.1 mg/L,135.6±21.1 mg/L vs 224.7±29.2 mg/L,均P<0.01),经SA-B干预后TGF-β1和TIMP-2表达明显下降,与模型组相比有显著性差异(18.53±2.54 vs 12.78±2.65,21.88±3.83 vs 14.69±4.51,均P<0.01),而MMP-2表达水平无明显变化.结论:SA-B能改善肝纤维化大鼠肝脏病理组织学结构,可能通过抑制TGF-β1和TIMP-2表达而促进肝纤维化的逆转.
