抗神经生长因子抗体用于改善子宫腺肌病小鼠宫腔内环境的研究

Improving internal environment of mouse uteri with adenomyosis by administration of anti-NGF

目的:探讨抗神经生长因子抗体(anti-NGF)对改善子宫腺肌病(AM)小鼠宫腔内环境的作用。方法:将15只雌性ICR小鼠随机分为AM治疗组(A组)、AM溶剂对照组(B组)及正常对照组(C组),A、B组使用口服他莫昔芬法建立AM小鼠模型。A组小鼠腹腔注射anti-NGF,B组以等体积的生理盐水替代,C组不作任何处理。3组小鼠于动情前期处死取双子宫称量后检测缓激肽受体1(BKR-1)、神经激肽1受体(NK-1R)、同源框基因转录因子A10(HOXA10)及芳香化酶(aromatase)基因与蛋白的表达。结果:A组子宫相对重量同B组,且均明显高于C组(P<0.05);A组BKR-1基因及蛋白和NK-1R基因水平较B组明显降低(P<0.05),与C组比较无统计学差异(P>0.05);A组HOXA10基因及蛋白水平较B组明显增高(P<0.05),与C组比较无统计学差异(P>0.05);A组芳香化酶基因及蛋白水平较B组减低(P<0.05),但仍高于C组(P<0.05)。结论:anti-NGF可显著缓解AM模型小鼠子宫炎症,改善内膜容受性、抑制芳香化酶表达,但短期使用不能抑制病灶增殖。

Objective： To explore the effect of anti-nerve growth factor（anti-NGF） on the uteri of adenomyosis（AM） mice. Methods： A total of 15 healthy and clean ICR mice were divided into 3 groups which were AM treatment group（group A）, AM placebo group（group B） and normal control group（group C） with 5 mice per group. ICR mice with AM（group A and group B） were induced by orally administration of tamoxifen. The mice in group A were intraperitoneal injected with rabbit anti-NGF antibody. The mice in three groups were killed at preoestrus and bilateral uteri were taken. The levels of mR NA and protein for bradykinin receptor 1（BKR-1）,neurokinin1 receptor（NK-1R）, homeobox A10（HOXA10） and aromatase were examined. Results： The uterine weight of group A and group B was significantly greater than that in group C（P〈0.05）, but there was no significant difference between group A and group B. The mR NA and protein level of BKR-1 and the mR NA level of NK-1R in group A were lower than those in group B（P〈0.05） and had no significant difference with group C. The mR NA and protein levels of HOXA10 in group A were higher than those in group B（P〈0.05） and had no difference with group C. The aromatase mR NA and protein levels of group A were lower than those in group B（P〈0.05）, but were higher than those in group C（P〈0.05）. Conclusion： Anti-NGF can significantly relieve inflammation in uteri of AM moden mice. It may play a role in improving endometrium receptivity, inhibiting the local estrogen synthesis.However, it plays no role in inhibiting the proliferation of AM lesions for short-term using.