背景:脑源性神经营养因子(BDNF)是各种慢性疾病中慢性疼痛发展和维持的已知调节剂。连同其高亲和力酪氨酸激酶B型(TrKB)受体,BDNF在哺乳动物雌性生殖系统中广泛表达。然而,BDNF和TrKB在子宫内膜异位症不同阶段的表达及各自在异位病灶中的表达与子宫内膜异位症疼痛的关系尚不清楚。
方法:本研究纳入62例接受腹腔镜手术的妇女:46例诊断为卵巢子宫内膜瘤(研究组),16例诊断为卵巢良性肿瘤(对照组)。在腹腔镜手术中获得来自在位子宫内膜和卵巢子宫内膜异位病变的样本。通过实时PCR和免疫组织化学染色检测两组在位和异位子宫内膜中的BDNF和TrKB信使RNA(mRNA)和蛋白水平,分别。手术前使用视觉模拟量表(VAS)测量痛经。
结果:BDNF和TrKB在卵巢子宫内膜异位病灶中的表达水平高于在位内膜和正常子宫内膜(P<0.05),也没有周期性的变化.此外,其在在位子宫内膜中的表达水平高于正常子宫内膜(P<0.05),Ⅳ期卵巢子宫内膜异位病灶的BDNF和TrKB水平高于Ⅱ期和Ⅲ期(P<0.05),III期的表达高于II期(P>0.05)。此外,在位子宫内膜BDNF或TrKBmRNA表达与痛经VAS评分的相关系数分别为r=0.52和r=0.56,分别为(P<0.05)。在位子宫内膜和异位子宫内膜中BDNF与TrKB的相关性分别为r=0.82和r=0.66(P<0.05)。
结论:BDNF和TrKB与子宫内膜异位症引起的痛经密切相关,可能在子宫内膜异位症的病理生物学或病理生理学中起重要作用。
BACKGROUND: Brain-derived neurotrophic factor (BDNF) is a known regulator of the development and maintenance of chronic pain in various chronic disorders. Together with its high-affinity tyrosine kinase type B (TrKB) receptor, BDNF is extensively expressed in the mammalian female reproductive system. However, BDNF and TrKB expression in different stages of endometriosis and the relationship between the expression of each in ectopic lesions and endometriosis pain remain unclear.
METHODS: Sixty-two women who underwent laparoscopic surgery were enrolled in this study: forty-six diagnosed with ovarian endometrioma (study group) and sixteen diagnosed with ovarian benign tumours (control group). Samples from eutopic endometrium and ovarian endometriotic lesions were obtained at laparoscopic surgery. BDNF and TrKB messenger RNA (mRNA) and proteins levels in the eutopic and ectopic endometrium of both groups were measured by real-time PCR and immunohistochemical staining, respectively. Before the surgery the visual analogue scale (VAS) was used to measure
dysmenorrhoea.
RESULTS: BDNF and TrKB expression levels were higher in ovarian endometriotic lesions than in eutopic endometrium and normal endometrium (P < 0.05), and there was no cyclical change. Furthermore, their expression levels were higher in eutopic endometrium than in normal endometrium (P < 0.05), and BDNF and TrKB levels were higher in stage IV ovarian endometriotic lesions than in stage II and III lesions (P < 0.05), with their expression being non-significantly higher in stage III than in stage II (P > 0.05). Additionally, correlation coefficients for the association analysis between the mRNA expression of BDNF or TrKB in eutopic endometrium and the
dysmenorrhoea VAS score were r = 0.52 and r = 0.56 for BDNF and TrKB, respectively (P < 0.05). The correlation coefficients for the associations between BDNF and TrKB in both the eutopic and ectopic endometrium were r = 0.82 and r = 0.66, respectively (P < 0.05).
CONCLUSIONS: BDNF and TrKB are closely related to
dysmenorrhoea caused by endometriosis and may be important in the pathobiology or pathophysiology of endometriosis.