中华临床医师杂志（电子版）
中華臨床醫師雜誌（電子版）
중화림상의사잡지（전자판）
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2014年
17期
3102-3106
,共5页
乔海风%刘颖蕾%鲁晓燕%王莹%刘宏斌%周金玲%刘曼华
喬海風%劉穎蕾%魯曉燕%王瑩%劉宏斌%週金玲%劉曼華
교해풍%류영뢰%로효연%왕형%류굉빈%주금령%류만화
巨噬细胞%白细胞介素6%子宫腺肌病%CD68
巨噬細胞%白細胞介素6%子宮腺肌病%CD68
거서세포%백세포개소6%자궁선기병%CD68
Macrophages%Interleukin-6%Adenomyosis%CD68
目的：探讨巨噬细胞CD68、IL-6子宫腺肌病发病机制的作用。方法采用免疫组化法检测巨噬细胞CD68、IL-6在58例子宫腺肌病病灶及结合带组织中的表达，以同期54例子宫肌瘤、30例子宫腺肌病合并肌瘤、30例CINⅢ为对照。结果（1）CD68、IL-6在子宫腺肌病病灶组织及结合带组织中的表达均高于其在子宫肌瘤及 CINⅢ组织中的表达，差异有统计学意义（P＜0.001）；（2）CD68、IL-6在子宫腺肌病病灶组织的表达高于其在腺肌病结合带组织的表达（P＜0.001）；（3）CD68、IL-6在子宫肌瘤病灶组织、结合带组织及CINⅢ结合带组织中的表达差异无统计学意义（P＞0.05）；（4）子宫腺肌病合并子宫肌瘤组CD68、IL-6在腺肌病病灶组织中的表达均高于其在肌瘤病灶组织中的表达，差异有统计学意义（P＜0.001）；（5）Pearson 相关分析显示：在子宫腺肌病病灶组织中CD68与IL-6的表达呈正相关（r＝0.303，P＝0.021）。结论巨噬细胞CD68与IL-6可能共同参与了子宫腺肌病的发生发展，在子宫腺肌病的发病机制中发挥着重要作用。
目的：探討巨噬細胞CD68、IL-6子宮腺肌病髮病機製的作用。方法採用免疫組化法檢測巨噬細胞CD68、IL-6在58例子宮腺肌病病竈及結閤帶組織中的錶達，以同期54例子宮肌瘤、30例子宮腺肌病閤併肌瘤、30例CINⅢ為對照。結果（1）CD68、IL-6在子宮腺肌病病竈組織及結閤帶組織中的錶達均高于其在子宮肌瘤及 CINⅢ組織中的錶達，差異有統計學意義（P＜0.001）；（2）CD68、IL-6在子宮腺肌病病竈組織的錶達高于其在腺肌病結閤帶組織的錶達（P＜0.001）；（3）CD68、IL-6在子宮肌瘤病竈組織、結閤帶組織及CINⅢ結閤帶組織中的錶達差異無統計學意義（P＞0.05）；（4）子宮腺肌病閤併子宮肌瘤組CD68、IL-6在腺肌病病竈組織中的錶達均高于其在肌瘤病竈組織中的錶達，差異有統計學意義（P＜0.001）；（5）Pearson 相關分析顯示：在子宮腺肌病病竈組織中CD68與IL-6的錶達呈正相關（r＝0.303，P＝0.021）。結論巨噬細胞CD68與IL-6可能共同參與瞭子宮腺肌病的髮生髮展，在子宮腺肌病的髮病機製中髮揮著重要作用。
목적：탐토거서세포CD68、IL-6자궁선기병발병궤제적작용。방법채용면역조화법검측거서세포CD68、IL-6재58례자궁선기병병조급결합대조직중적표체，이동기54례자궁기류、30례자궁선기병합병기류、30례CINⅢ위대조。결과（1）CD68、IL-6재자궁선기병병조조직급결합대조직중적표체균고우기재자궁기류급 CINⅢ조직중적표체，차이유통계학의의（P＜0.001）；（2）CD68、IL-6재자궁선기병병조조직적표체고우기재선기병결합대조직적표체（P＜0.001）；（3）CD68、IL-6재자궁기류병조조직、결합대조직급CINⅢ결합대조직중적표체차이무통계학의의（P＞0.05）；（4）자궁선기병합병자궁기류조CD68、IL-6재선기병병조조직중적표체균고우기재기류병조조직중적표체，차이유통계학의의（P＜0.001）；（5）Pearson 상관분석현시：재자궁선기병병조조직중CD68여IL-6적표체정정상관（r＝0.303，P＝0.021）。결론거서세포CD68여IL-6가능공동삼여료자궁선기병적발생발전，재자궁선기병적발병궤제중발휘착중요작용。
ObjectiveTo explore the roles of macrophage and IL-6 in the pathogenesis of adenomyosis(AM).MethodsThe CD68 is employed to mark macrophages, immunohistochemical staining were used to detect the expression of CD68 and IL-6 in ectopic endometrial and junction zone specimens in 58 cases of patients with adenomyosis, compared with 54 cases of patients with leiomyoma, 30 cases of patients with adenomyosis associated with leiomyoma, and 30 cases of patients with CINⅢ. ResultsThe expression of CD68 and IL-6 in ectopic endometrial and junction zone specimens in AM group were significantly higher than that in leiomyoma group and CINⅢ group (P<0.001). The expression of CD68 and IL-6 in ectopic endometrial in AM were significantly higher than that in junction zone (P<0.001). The expression of CD68 and IL-6 didn't show significant difference between leiomyoma group and CINⅢ (P>0.05), and so between myoma tissue samples and junction zone in leiomyoma group (P>0.05). The expression of CD68 and IL-6 in adenomyoma tissues were significantly higher than that in myoma tissues in 30 cases of patients with adenomyosis associated with leiomyoma (P<0.001). The expression of CD68 in eutopic endometrial in adenomyosis was positively correlated with the number of IL-6 (r=0.303,P=0.021).ConclusionMacrophage and IL-6 may play an important role in the pathogenesis of AM.
