单核细胞趋化蛋白-1、基质细胞衍生因子-1在子宫腺肌病中的表达及意义
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摘要
目的：探讨单核细胞趋化蛋白-1(monocyte chemoattractant protein-1, MCP-1)在子宫腺肌病发病中的作用。
方法：采用免疫组化法和实时荧光定量PCR法检测36例子宫腺肌病患者在位内膜、病灶周围组织和异位灶组织中MCP-1的含量,并与相应对照组进行比较。
结果：1.MCP-1蛋白的表达：腺肌病异位灶中MCP-1蛋白的表达显著高于在位内膜和对照内膜(p<0.05)；在位内膜显著高于对照内膜(p<0.05)；各分组内增殖期和分泌期MCP-1蛋白的表达没有统计学差异(p>0.05)。
相关性分析表明：MCP-1蛋白表达在位内膜与异位灶之间具有显著相关性(r=0.870,P<0.05)。
2. MCP-1mRNA含量的比较：腺肌病组在位内膜、病灶周围组织和异位灶组织中MCP-1mRNA的含量均高于相应对照组,差异均具有统计学意义(p<0.05)；腺肌病异位灶与在位内膜和病灶周围组织相比,MCP-1mRNA的含量显著增高(p<0.05)；MCP-1mRNA的含量在在位内膜、病灶周围组织和异位灶组织呈递增趋势。不管是在位内膜还是对照内膜,增殖期与分泌期比较,MCP-1mRNA的含量差异均没有统计学意义(p>0.05)。
直线相关分析显示：在位内膜与病灶周围组织、在位内膜与异位灶、病灶周围组织与异位灶之间,均具有显著相关性(r=0.499,P<0.05；r=0.461,P<0.05；r=0.679,P<0.05)。
结论：1、MCP-1在子宫腺肌病的发生、发展过程中起一定作用；
2、MCP-1可能通过改变局部微环境的免疫状态参与子宫腺肌病的发病过程；
3、检测局部内膜组织中MCP-1的表达,可能会有助于早期诊断子宫腺肌病；
4、从分子生物学角度为子宫腺肌病保守性手术后容易出现复发,应辅以药物治疗提供了佐证。
目的：探讨趋化因子CXCL12,即基质细胞衍生因子-1(stromal cell derived factor-1,SDF-1)在子宫腺肌病发病中的作用。
方法：采用免疫组化法和实时荧光定量PCR法检测36例子宫腺肌病患者在位内膜、病灶周围组织和异位灶组织中CXCL12的表达,并与相应对照组进行比较。
结果：1.CXCL12蛋白的表达：腺肌病异位灶CXCL12蛋白的表达显著高于在位内膜和对照内膜(p<0.05),在位内膜显著高于对照内膜(p<0.05),各分组内增殖期和分泌期CXCL12蛋白的表达没有统计学差异(p>0.05)。
相关性分析表明：CXCL12蛋白的表达在位内膜与异位灶之间具有显著相关性(r=0.780,P<0.05)。
2. CXCL12mRNA的含量：腺肌病组在位内膜、病灶周围组织和异位灶组织中CXCL12mRNA的含量均高于相应对照组,差异均具有统计学意义(p<0.05)；腺肌病异位灶与在位内膜和病灶周围组织相比,CXCL12mRNA的含量显著增高(p<0.05)；CXCL12mRNA的含量在在位内膜、病灶周围组织和异位灶呈递增趋势。不管是在位内膜还是对照内膜,增殖期CXCL12mRNA的含量均高于分泌期,但无统计学差异(p>0.05)。
直线相关分析显示：CXCL12mRNA含量在位内膜与病灶周围组织、在位内膜与异位灶、病灶周围组织与异位灶之间,均具有显著相关性(r=0.466,P<0.05；r=0.553,P<0.05：r=0.577,P<0.05)。
3.MCP-1和CXCL12的相关性分析：在位内膜和异位灶组织中,MCP-1和CXCL12蛋白的表达存在显著相关性(r在位内膜=0.486,p<0.05；r异位灶=0.612,p<0.05)；在位内膜、病灶周围组织和异位灶组织中,MCP-1mRNA和CXCL12mRNA的含量变化均存在显著相关性(r在位内膜=0.493,p<：0.05；rv病灶周围组织=0.439,p<0.05；r异位灶=0.520,p<0.05)。
结论：1、CXCL12在子宫腺肌病发生、发展过程中起一定作用；
2、CXCL12可能通过溶解局部细胞外基质,促进局部微血管形成,诱导内膜细胞沿浓度梯度迁移等参与子宫腺肌病的发病过程；
3、检测局部内膜组织中CXCL12含量的变化,可能会有助于早期诊断子宫腺肌病：
4、从分子生物学角度为子宫腺肌病保守性手术后容易出现复发,保守性手术后应辅以药物治疗提供了依据；
5, MCP-1、CXCL12在子宫腺肌病的发病过程中具有协同作用；
6、趋化因子CXCL12及其受体CXCR4有可能成为腺肌病治疗的一个非常有意义靶点。
目的：探讨米非司酮在预防子宫腺肌病发病中的作用。
方法：采用免疫组化法和实时荧光定量PCR法检测30例子宫腺肌病患者服用米非司酮后在位内膜组织中MCP-1、CXCL12的含量变化。
结果：1、MCP-1蛋白表达的变化：治疗后组显著低于治疗前组(p<0.05)；
2、CXCL12蛋白表达的变化：治疗后组显著低于治疗前组(p<0.05)；
3、MCP-1mRNA含量的变化：治疗后组显著低于治疗前组(p<0.05)；
4、CXCL12mRNA含量的变化：治疗后组显著低于治疗前组(p<0.05)。
结论：1、米非司酮抑制了腺肌病在位内膜组织中MCP-1和CXCL12的表达；
2、米非司酮通过抑制在位内膜组织中某些与腺肌病发生有关的细胞因子的合成与释放,可能在预防子宫腺肌病的发生中发挥作用；
3、子宫内膜损伤后,小剂量、短疗程服用米非司酮(10mg/天,连续30天),可能会预防子宫腺肌病的发生,但临床应用和效果仍需要进一步深入地研究；
4、子宫腺肌病保守性手术后可辅以米非司酮防止病变复发,但具体用药剂量和用药时间尚需要进一步临床研究论证。
Objective:To investigate the role of monocyte chemoattractant protein-1(MCP-1) in the pathogenesis of adenomyosis.
Methods:MCP-1was detected by immunohistochemistry and Real-Time PCR in eutopic endometrium,ectopic endometrium and surrounding the lesion tissue of36adenomyosis cases,and compared with the corresponding controls.
Results:1.Expression of MCP-1protein:MCP-1protein expression in adenomyosis ectopic lesions was significantly higher than that in eutopic endometrium and control endometrium (P<0.05); MCP-1protein expression in eutopic endometrium was significantly higher than that in control endometrium (P<0.05); MCP-1protein expression in various subgroups within the proliferative and secretory phase were not statistically different (P>0.05).
Correlation analysis showed that MCP-1protein expression in eutopic endometrium and ectopic lesions have significant correlation (r=0.87, P<0.05).
2.MCP-1mRNA content comparison:MCP-1mRNA content in adenomyosis group of eutopic endometrium, surrounding the lesion tissue and ectopic lesion tissue were higher than that in the corresponding controls,the differences have statistical significance (P<0.05);Adenomyosis ectopic lesions compared with eutopic endometrium and the lesion of the peripheral tissues, MCP-1mRNA content remarkably increased (P<0.05);MCP-1content in eutopic endometrium, lesions in the peripheral tissues and ectopic lesions showed increasing trend.Whether in eutopic endometrium and control endometrium,MCP-1content of proliferative and secretory phase were not statistically significant (P>0.05).
Linear correlation analysis showed that MCP-1mRNA content in eutopic endometrial lesions and surrounding tissues,eutopic endometrium and ectopic lesions,lesions in the peripheral tissues and ectopic lesions have significant correlation (P<0.05).
Conclusions:
1. MCP-1is involved in the pathogenesis of adenomyosis;
2. MCP-1may change the local microenvironment of immune state in the pathogenesis of adenomyosis;
3. The detection of MCP-1content in eutopic endometrium may contribute to the early diagnosis of adenomyosis;
4. Provide molecular evidence for adenomyosis recurrence after conservative operation. Adenomyosis after conservative operation should combined with drug therapy.
Objective:To investigate the chemotactic factor CXCL12,namely the stromal cell derived factor1(SDF-1) in the pathogenesis of uterine adenomyosis.
Methods:Using immunohistochemical method and Real-Time PCR assay for detection of CXCL12content in eutopic endometrium,ectopic endometrium and surrounding the lesion tissues of36cases of uterine adenomyosis,and compared with the corresponding control groups.
Results:1. CXCL12protein expression:CXCL12protein expression in adenomyosis ectopic lesions was significantly higher than that in eutopic endometrium and control endometrium (P<0.05),eutopic endometrium was significantly higher than that in control endometrium (P<0.05).CXCL12protein expression in various subgroups within the proliferative and secretory phase were not statistically different (P>0.05).
Correlation analysis showed that CXCL12protein expression in eutopic endometrium and ectopic lesions have significant correlation (r=0.78, P<0.05).
2. CXCL12mRNA content:CXCL12mRNA content in adenomyosis group of eutopic endometrium, surrounding the lesion tissue and ectopic lesion tissue were higher than that in the corresponding controls,the differences have statistical significance (P<0.05);Adenomyosis ectopic lesion tissue compared with eutopic endometrium and the lesion of the peripheral tissues,CXCL12mRNA content remarkably increased(P<0.05);The content of CXCL12mRNA in eutopic endometrium lesions,in the peripheral tissues and ectopic lesions showed increasing trend.Whether in the eutopic endometrium or in control endometrium, CXCL12mRNA content in proliferative phase were higher than that in the secretory phase,but showed no significant difference (P>0.05).
Linear correlation analysis showed that the CXCLI2mRNA content in eutopic endometrium and lesions in the peripheral tissues,eutopic endometrium and ectopic lesions,lesions in the peripheral tissues and ectopic lesions have significant correlation (P<0.05).
3. MCP-1and CXCL12correlation analysis:MCP-1and CXCL12protein expression in eutopic endometrium and ectopic foci were significantly correlated(reutopic endometrium=0.486,p<0.05; rectopic foci=0.612,p<0.05);MCP-1mRNA and CXCL12mRNA content in eutopic endometrium,surrounding the lesion tissue and ectopic foci showed significant correlation (reutopic endometrium=0.493, p<0.05; rsurrounding the lesion tissue=0.439, p<0.05; rectopic foci=0.520, p<0.05).
Conclusion:
1.CXCL12is involved in the pathogenesis of adenomyosis;
2.CXCL12may be through dissolve local extracellular matrix,promote local microvessel formation, participate the pathogenesis of adenomyosis;
3.The detection of CXCL12content in eutopic endometrium may contribute to the early diagnosis of adenomyosis;
4.Provide molecular evidence for adenomyosis recurrence after conservative operation. Adenomyosis after conservative operation should combined with drug therapy;
5.MCP-1and CXCL12have synergistic effect during the pathogenesis of adenomyosis;
6. Chemotactic factor CXCL12and its receptor CXCR4may become a very meaningful targets for adenomyosis treatment, which need further research.
Objective:To investigate the prevention role of mifepristone on pathogenesis of uterine adenomyosis.
Methods:Using immunohistochemical method and Real-Time PCR assay for detection of MCP-1and CXCL12content in the uterus endometrial tissue of30patients with adenomyosis after taking mifepristone, and compared with that before taking mifepristone.
Results:MCP-1, CXCL12protein expression and mRNA content in endometrial tissue of patients with adenomyosis after mifepristone treatment were lower than that before treatment(P<0.05).
Conclusion:
1.Mifepristone inhibits MCP-1and CXCL12expression in adenomyosis eutopic endometrial tissue;
2.Mifepristone may prevent uterine adenomyosis by inhibiting some cytokine synthesis and release associated with adenomyosis in the eutopic endometrial tissue;
3.Taking mifepristone with little dosage, short course (10mg/day,30consecutive days) after injury of the endometrium may prevent the occurrence of uterine adenomyosis, its clinical effect still needs further study;
4.Adenomyosis after conservative operation can be supplemented with mifepristone to prevent recurrence, the specific dosage and duration of medication needs further clinical studies.
方法：采用免疫组化法和实时荧光定量PCR法检测36例子宫腺肌病患者在位内膜、病灶周围组织和异位灶组织中MCP-1的含量,并与相应对照组进行比较。
结果：1.MCP-1蛋白的表达：腺肌病异位灶中MCP-1蛋白的表达显著高于在位内膜和对照内膜(p<0.05)；在位内膜显著高于对照内膜(p<0.05)；各分组内增殖期和分泌期MCP-1蛋白的表达没有统计学差异(p>0.05)。
相关性分析表明：MCP-1蛋白表达在位内膜与异位灶之间具有显著相关性(r=0.870,P<0.05)。
2. MCP-1mRNA含量的比较：腺肌病组在位内膜、病灶周围组织和异位灶组织中MCP-1mRNA的含量均高于相应对照组,差异均具有统计学意义(p<0.05)；腺肌病异位灶与在位内膜和病灶周围组织相比,MCP-1mRNA的含量显著增高(p<0.05)；MCP-1mRNA的含量在在位内膜、病灶周围组织和异位灶组织呈递增趋势。不管是在位内膜还是对照内膜,增殖期与分泌期比较,MCP-1mRNA的含量差异均没有统计学意义(p>0.05)。
直线相关分析显示：在位内膜与病灶周围组织、在位内膜与异位灶、病灶周围组织与异位灶之间,均具有显著相关性(r=0.499,P<0.05；r=0.461,P<0.05；r=0.679,P<0.05)。
结论：1、MCP-1在子宫腺肌病的发生、发展过程中起一定作用；
2、MCP-1可能通过改变局部微环境的免疫状态参与子宫腺肌病的发病过程；
3、检测局部内膜组织中MCP-1的表达,可能会有助于早期诊断子宫腺肌病；
4、从分子生物学角度为子宫腺肌病保守性手术后容易出现复发,应辅以药物治疗提供了佐证。
目的：探讨趋化因子CXCL12,即基质细胞衍生因子-1(stromal cell derived factor-1,SDF-1)在子宫腺肌病发病中的作用。
方法：采用免疫组化法和实时荧光定量PCR法检测36例子宫腺肌病患者在位内膜、病灶周围组织和异位灶组织中CXCL12的表达,并与相应对照组进行比较。
结果：1.CXCL12蛋白的表达：腺肌病异位灶CXCL12蛋白的表达显著高于在位内膜和对照内膜(p<0.05),在位内膜显著高于对照内膜(p<0.05),各分组内增殖期和分泌期CXCL12蛋白的表达没有统计学差异(p>0.05)。
相关性分析表明：CXCL12蛋白的表达在位内膜与异位灶之间具有显著相关性(r=0.780,P<0.05)。
2. CXCL12mRNA的含量：腺肌病组在位内膜、病灶周围组织和异位灶组织中CXCL12mRNA的含量均高于相应对照组,差异均具有统计学意义(p<0.05)；腺肌病异位灶与在位内膜和病灶周围组织相比,CXCL12mRNA的含量显著增高(p<0.05)；CXCL12mRNA的含量在在位内膜、病灶周围组织和异位灶呈递增趋势。不管是在位内膜还是对照内膜,增殖期CXCL12mRNA的含量均高于分泌期,但无统计学差异(p>0.05)。
直线相关分析显示：CXCL12mRNA含量在位内膜与病灶周围组织、在位内膜与异位灶、病灶周围组织与异位灶之间,均具有显著相关性(r=0.466,P<0.05；r=0.553,P<0.05：r=0.577,P<0.05)。
3.MCP-1和CXCL12的相关性分析：在位内膜和异位灶组织中,MCP-1和CXCL12蛋白的表达存在显著相关性(r在位内膜=0.486,p<0.05；r异位灶=0.612,p<0.05)；在位内膜、病灶周围组织和异位灶组织中,MCP-1mRNA和CXCL12mRNA的含量变化均存在显著相关性(r在位内膜=0.493,p<：0.05；rv病灶周围组织=0.439,p<0.05；r异位灶=0.520,p<0.05)。
结论：1、CXCL12在子宫腺肌病发生、发展过程中起一定作用；
2、CXCL12可能通过溶解局部细胞外基质,促进局部微血管形成,诱导内膜细胞沿浓度梯度迁移等参与子宫腺肌病的发病过程；
3、检测局部内膜组织中CXCL12含量的变化,可能会有助于早期诊断子宫腺肌病：
4、从分子生物学角度为子宫腺肌病保守性手术后容易出现复发,保守性手术后应辅以药物治疗提供了依据；
5, MCP-1、CXCL12在子宫腺肌病的发病过程中具有协同作用；
6、趋化因子CXCL12及其受体CXCR4有可能成为腺肌病治疗的一个非常有意义靶点。
目的：探讨米非司酮在预防子宫腺肌病发病中的作用。
方法：采用免疫组化法和实时荧光定量PCR法检测30例子宫腺肌病患者服用米非司酮后在位内膜组织中MCP-1、CXCL12的含量变化。
结果：1、MCP-1蛋白表达的变化：治疗后组显著低于治疗前组(p<0.05)；
2、CXCL12蛋白表达的变化：治疗后组显著低于治疗前组(p<0.05)；
3、MCP-1mRNA含量的变化：治疗后组显著低于治疗前组(p<0.05)；
4、CXCL12mRNA含量的变化：治疗后组显著低于治疗前组(p<0.05)。
结论：1、米非司酮抑制了腺肌病在位内膜组织中MCP-1和CXCL12的表达；
2、米非司酮通过抑制在位内膜组织中某些与腺肌病发生有关的细胞因子的合成与释放,可能在预防子宫腺肌病的发生中发挥作用；
3、子宫内膜损伤后,小剂量、短疗程服用米非司酮(10mg/天,连续30天),可能会预防子宫腺肌病的发生,但临床应用和效果仍需要进一步深入地研究；
4、子宫腺肌病保守性手术后可辅以米非司酮防止病变复发,但具体用药剂量和用药时间尚需要进一步临床研究论证。
Objective:To investigate the role of monocyte chemoattractant protein-1(MCP-1) in the pathogenesis of adenomyosis.
Methods:MCP-1was detected by immunohistochemistry and Real-Time PCR in eutopic endometrium,ectopic endometrium and surrounding the lesion tissue of36adenomyosis cases,and compared with the corresponding controls.
Results:1.Expression of MCP-1protein:MCP-1protein expression in adenomyosis ectopic lesions was significantly higher than that in eutopic endometrium and control endometrium (P<0.05); MCP-1protein expression in eutopic endometrium was significantly higher than that in control endometrium (P<0.05); MCP-1protein expression in various subgroups within the proliferative and secretory phase were not statistically different (P>0.05).
Correlation analysis showed that MCP-1protein expression in eutopic endometrium and ectopic lesions have significant correlation (r=0.87, P<0.05).
2.MCP-1mRNA content comparison:MCP-1mRNA content in adenomyosis group of eutopic endometrium, surrounding the lesion tissue and ectopic lesion tissue were higher than that in the corresponding controls,the differences have statistical significance (P<0.05);Adenomyosis ectopic lesions compared with eutopic endometrium and the lesion of the peripheral tissues, MCP-1mRNA content remarkably increased (P<0.05);MCP-1content in eutopic endometrium, lesions in the peripheral tissues and ectopic lesions showed increasing trend.Whether in eutopic endometrium and control endometrium,MCP-1content of proliferative and secretory phase were not statistically significant (P>0.05).
Linear correlation analysis showed that MCP-1mRNA content in eutopic endometrial lesions and surrounding tissues,eutopic endometrium and ectopic lesions,lesions in the peripheral tissues and ectopic lesions have significant correlation (P<0.05).
Conclusions:
1. MCP-1is involved in the pathogenesis of adenomyosis;
2. MCP-1may change the local microenvironment of immune state in the pathogenesis of adenomyosis;
3. The detection of MCP-1content in eutopic endometrium may contribute to the early diagnosis of adenomyosis;
4. Provide molecular evidence for adenomyosis recurrence after conservative operation. Adenomyosis after conservative operation should combined with drug therapy.
Objective:To investigate the chemotactic factor CXCL12,namely the stromal cell derived factor1(SDF-1) in the pathogenesis of uterine adenomyosis.
Methods:Using immunohistochemical method and Real-Time PCR assay for detection of CXCL12content in eutopic endometrium,ectopic endometrium and surrounding the lesion tissues of36cases of uterine adenomyosis,and compared with the corresponding control groups.
Results:1. CXCL12protein expression:CXCL12protein expression in adenomyosis ectopic lesions was significantly higher than that in eutopic endometrium and control endometrium (P<0.05),eutopic endometrium was significantly higher than that in control endometrium (P<0.05).CXCL12protein expression in various subgroups within the proliferative and secretory phase were not statistically different (P>0.05).
Correlation analysis showed that CXCL12protein expression in eutopic endometrium and ectopic lesions have significant correlation (r=0.78, P<0.05).
2. CXCL12mRNA content:CXCL12mRNA content in adenomyosis group of eutopic endometrium, surrounding the lesion tissue and ectopic lesion tissue were higher than that in the corresponding controls,the differences have statistical significance (P<0.05);Adenomyosis ectopic lesion tissue compared with eutopic endometrium and the lesion of the peripheral tissues,CXCL12mRNA content remarkably increased(P<0.05);The content of CXCL12mRNA in eutopic endometrium lesions,in the peripheral tissues and ectopic lesions showed increasing trend.Whether in the eutopic endometrium or in control endometrium, CXCL12mRNA content in proliferative phase were higher than that in the secretory phase,but showed no significant difference (P>0.05).
Linear correlation analysis showed that the CXCLI2mRNA content in eutopic endometrium and lesions in the peripheral tissues,eutopic endometrium and ectopic lesions,lesions in the peripheral tissues and ectopic lesions have significant correlation (P<0.05).
3. MCP-1and CXCL12correlation analysis:MCP-1and CXCL12protein expression in eutopic endometrium and ectopic foci were significantly correlated(reutopic endometrium=0.486,p<0.05; rectopic foci=0.612,p<0.05);MCP-1mRNA and CXCL12mRNA content in eutopic endometrium,surrounding the lesion tissue and ectopic foci showed significant correlation (reutopic endometrium=0.493, p<0.05; rsurrounding the lesion tissue=0.439, p<0.05; rectopic foci=0.520, p<0.05).
Conclusion:
1.CXCL12is involved in the pathogenesis of adenomyosis;
2.CXCL12may be through dissolve local extracellular matrix,promote local microvessel formation, participate the pathogenesis of adenomyosis;
3.The detection of CXCL12content in eutopic endometrium may contribute to the early diagnosis of adenomyosis;
4.Provide molecular evidence for adenomyosis recurrence after conservative operation. Adenomyosis after conservative operation should combined with drug therapy;
5.MCP-1and CXCL12have synergistic effect during the pathogenesis of adenomyosis;
6. Chemotactic factor CXCL12and its receptor CXCR4may become a very meaningful targets for adenomyosis treatment, which need further research.
Objective:To investigate the prevention role of mifepristone on pathogenesis of uterine adenomyosis.
Methods:Using immunohistochemical method and Real-Time PCR assay for detection of MCP-1and CXCL12content in the uterus endometrial tissue of30patients with adenomyosis after taking mifepristone, and compared with that before taking mifepristone.
Results:MCP-1, CXCL12protein expression and mRNA content in endometrial tissue of patients with adenomyosis after mifepristone treatment were lower than that before treatment(P<0.05).
Conclusion:
1.Mifepristone inhibits MCP-1and CXCL12expression in adenomyosis eutopic endometrial tissue;
2.Mifepristone may prevent uterine adenomyosis by inhibiting some cytokine synthesis and release associated with adenomyosis in the eutopic endometrial tissue;
3.Taking mifepristone with little dosage, short course (10mg/day,30consecutive days) after injury of the endometrium may prevent the occurrence of uterine adenomyosis, its clinical effect still needs further study;
4.Adenomyosis after conservative operation can be supplemented with mifepristone to prevent recurrence, the specific dosage and duration of medication needs further clinical studies.
引文
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