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目的:探讨Toll样受体4(TLR4)信号活化内膜间质在腺肌症发生与发展中的调控作用。方法:Western blot法检测腺肌病在位子宫内膜及病灶内膜中TLR4表达情况;建立原代间质体系,lipopolysaccharide(LPS)刺激靶细胞,CCK-8技术观察细胞增殖活力;Western blot法检测TLR4核心信号表达;Western blot法和酶联免疫吸附测定(ELISA)技术检测和分析间质细胞炎性增殖及侵袭生长相关因子表达;采用TLR4拮抗剂VIPER处理细胞,验证TLR4信号对间质生物效应的影响。结果:TLR4表达于细胞质膜,在腺肌症病灶内膜中表达最高;LPS刺激使间质细胞活力增强、TLR4核心信号及增殖侵袭因子表达增加;VIPER可抑制上述因子表达。结论:LPS/TLR4信号活促进内膜间质细胞炎性增殖、侵袭生长,在子宫腺肌症发病中发挥重要作用,提示宫腔感染可能与腺肌病发病具有一定的相关性。
Objective: To investigate the regulatory role of Toll-like receptor 4 (TLR4) signaling in the activation and progression of adenomyosis. Methods: The expression of TLR4 in eutopic endometrium and focal intima of adenomyosis was detected by Western blot. The primary stromal system was established and target cells were stimulated by lipopolysaccharide (LPS). Cell viability was detected by CCK-8. The expression of TLR4 core signal was detected by Western blot and enzyme-linked immunosorbent assay (ELISA), and the expression of TLR4-VIPER was detected and analyzed. The expression of TLR4 signal on interstitial cells Effect of the effect. Results: TLR4 was expressed in the plasma membrane and highest in the intima of focal adenomyosis. LPS stimulated the proliferation of stromal cells and the expression of TLR4 core signal and proliferative invasion factor. VIPER inhibited the expression of TLR4. CONCLUSION: LPS / TLR4 signaling promotes endometrial stromal inflammatory proliferation, invasion and growth and plays an important role in the pathogenesis of adenomyosis, suggesting that intrauterine infection may be related to the development of adenomyosis.