Adenomyosis (AM) is an estrogen-dependent gynecological disorder in which local steroid handling may contribute to clinical heterogeneity. To characterize estrogen metabolic features in AM, we used liquid chromatography-tandem mass spectrometry (LC-MS/MS) to quantify 13 estrogens and estrogen metabolites in endometrial tissue and serum. Tissue metabolite profiles showed marked increases in catechol estrogens, particularly 2-hydroxyestrone (2-OHE1) and 4-hydroxyestrone (4-OHE1), whereas serum changes were more limited, with 2-methoxyestrone (2-MeOE1) representing the main circulating difference. Pathway- and ratio-based analyses indicated enhanced hydroxylation in tissue without a proportionate increase in downstream methylation-related readouts. Correlation and regression analyses further showed that tissue 2-OHE1 and 4-OHE1 were independently associated with dysmenorrhea severity. In exploratory receiver operating characteristic analyses performed within the discovery cohort, tissue catechol estrogens showed stronger discriminatory ability than serum metabolites. These findings suggested that AM was associated with endometrial tissue-predominant remodeling of estrogen metabolism rather than with generalized elevation of parent estrogens. The present study identified candidate metabolic markers requiring further validation and provided a framework for future investigation of local steroid metabolism in AM.

Background:Endometriosis-associated infertility (EAI) has emerged as an increasingly pressing reproductive health problem. Nevertheless, existing epidemiological research on EAI remains inadequate. Methods:This study integrated the Global Burden of Disease (GBD) 2023 data and single-center clinical data. We analyzed time trends in prevalence and years lived with disability (YLDs) of EAI in China, Japan, and the Republic of Korea. For China, we conducted age-period-cohort analysis and adopted the Bayesian age-period-cohort model to forecast disease burden trends up to 2030. Clinical data from a single center were used to compare age, BMI, and surgical stage among EAI subgroups. Results:In 2023, the number of prevalent cases of EAI in China was 181587 (95% UI: 114233, 278960), with the age-standardized prevalence rate (ASPR) of 26.38 (95% UI: 16.45, 39.91) per 100,000 population. Although the overall ASPR of EAI in China showed a downward trend from 1990 to 2023, with an average annual percent change of -0.57% (95% CI: -0.80, -0.43), an increase was observed during the recent period from 2021 to 2023, with an annual percent change of 9.75% (95% CI: 4.06, 13.51). Trends in YLDs were consistent with prevalence patterns. ASPR and prevalent cases are projected to rise through 2030. Both GBD and real-world data identified a peak in secondary infertility at ages 35-39; for primary infertility, the peak age was 20-24 years based on GBD data and 25-29 years according to real-world data. Secondary infertility is the predominant type, and most patients were classified as the American Society for Reproductive Medicine (ASRM) stage III. Conclusion:The recent rebound in EAI burden reveals a growing hidden threat to female reproductive health. Its upward trend is expected to continue to 2030. Early screening for primary infertility in women aged 20-29 years and targeted management of secondary infertility in those aged 35-39 years are warranted.

Adenomyosis (AM), a gynecological disorder that severely affects female reproductive health. AM-associated macrophage (AAM) polarization-induced epithelial–mesenchymal transition (EMT) is a key driver of AM progression. In this study, we investigated the role and underlying mechanisms of endometrial mesenchymal stem cell (eMSC)-derived exosomes in regulating AAM polarization and the subsequent EMT of endometrial epithelial cells (EECs). In vitro coculture studies revealed that AM eutopic eMSCs markedly induced M2 macrophage polarization via exosomes and promoted EMT of EECs. Differentially expressed microRNAs (DE-miRNAs) between exosomes derived from normal eMSCs (N-eMSCs) and AM eutopic eMSCs (A-eMSCs) were identified using miRNA sequencing and miR-4669 was found to be the most significantly upregulated miRNA. Internalization of exosomal miR-4669 by macrophages induced their polarization toward the M2 phenotype and promoted the EMT of EECs. Mechanistic analysis using luciferase assay, mRNA sequencing, and rescue experiments revealed that miR-4669 induced M2 macrophage polarization via downregulation of DUSP6 and activation of MAPK/ERK signaling. The polarized M2 macrophages promoted the EMT of ISK cells via TGF-β1 secretion. In an AM xenograft mouse model, miR-4669 depletion inhibited AM progression by targeting the DUSP6/ERK1/2 pathway in macrophages. Overall, AM A-eMSC-derived exosomal miR-4669 facilitates M2 macrophage polarization by targeting the DUSP6/ERK signaling pathway, thereby promoting EMT of EECs via TGF-β1 secretion. These findings open avenues for developing novel preventive and therapeutic strategies for AM.

Endometriosis, a persistent inflammatory disease, is associated with pelvic or abdominal pain. The immune system and sensory nervous system show a synergistic effect on regulation of pain. In particular, Interleukin-33 (IL-33) is released as a danger signal and drives key hallmarks of severe endometriosis. To explore the mechanistic involvement of IL-33 in pain associated with endometriosis, both an in vivo murine endometriosis model and in vitro experiments with RAW 264.7 cells and dorsal root ganglion (DRG) neurons were utilized. In vivo, we demonstrated that IL-33 significantly exacerbated endometriosis and induced hyperalgesia in mice. By interacting with the ST2 receptor in macrophages, IL-33 enhanced the release of tumor necrosis factor α (TNF-α) and Interleukin 1β (IL-1β). This process set off an inflammatory cascade, which further facilitated macrophages recruitment and neurogenesis in ectopic lesions. As an ion channel expressed by nociceptors, transient receptor potential vanilloid 1 (TRPV1) expression was significantly increased in DRG in the presence of IL-33. In vitro, we confirmed that IL-33 elevated the release of TNF-α in macrophages. Ultimately, macrophage-derived TNF-α increased TRPV1 protein level in DRG neuronal cells through the TNFR1/p38 MAPK signaling pathway. Overall, these results revealed an inductive role of IL-33 in pain associated with endometriosis, and highlighted the interaction between macrophages and sensory neurons.

BACKGROUND:The clinical management of ischemic disease and cancer is complex, with disruptions in local vascular function and tumor angiogenesis contributing to blood stasis, which complicates treatment strategies. Salvia miltiorrhiza, a natural product, is known to restore vascular structure and function. However, its specific roles in concurrently addressing ischemic disease and cancer within the same organism remain poorly understood. PURPOSE:This study aimed to explore the material basis, pharmacological effects, and underlying mechanisms of Salvia miltiorrhiza extract (SME) in promoting blood flow recovery in ischemic hindlimbs and inducing tumor vascular normalization. METHODS:The pharmacological effects of SME were evaluated in a mouse model combining ischemic hindlimbs and tumors. Mice were administered low (SME-L) or high (SME-H) doses of SME daily, and the gastrocnemius muscle mass and tumor vascular structure were assessed. Laser Doppler perfusion imaging (LDPI) was used to monitor hindlimb blood flow recovery and tumor vascular perfusion. The pharmacokinetics of the key bioactive constituents in SME were characterized by liquid chromatography-mass spectrometry (LC-MS). Interactions between SME's active compounds and predicted targets were investigated using molecular docking, microscale thermophoresis (MST), and luciferase reporter assays. The synergistic effects of the primary components, Tanshinone I (Tan I) and Salvianolic acid A (Sal A), were analyzed through tube formation assays, enzyme-linked immunosorbent assays (ELISA), immunofluorescence staining, and western blot. RESULTS:Phytochemical profiling revealed that SME contains several active compounds, including Danshensu, Sal A, Sal B, Tan IIA, and Tan I. SME treatment reduced the frequency of necrotic toes, increased muscle mass, and alleviated hypoxia in the gastrocnemius muscle. SME significantly improved tumor vascular perfusion and notably enhanced pericyte coverage and basement membrane integrity. Pharmacokinetic analysis identified Tan I and Sal A as the key bioactive components that promote vascular normalization. Tan I inhibited FoxO1, preventing endothelial cell activation induced by angiopoietin 2 (Ang2), while Sal A bound to Ang2, facilitating Tie2 activation mediated by Ang1. Both in vitro and in vivo results demonstrated that the combination of Tan I and Sal A exerted a synergistic therapeutic effect on correcting abnormal blood vessels in ischemic hindlimbs and tumors. CONCLUSION:Our study innovatively revealed a reliable mouse model wherein the Ang2/Tie2 signaling cascade disrupted the endothelial homeostasis to aggravate the progression of hindlimb ischemia and tumor angiogenesis. This balance can be rescued by the combination therapy of Tan I and Sal A that were both from SME, leading to the occurrence of vascular normalization.

Adenomyosis (AM) is a common non-cancerous condition of the uterus that has significant effects on women's health. Despite its clinical importance, the advancement of dependable non-invasive diagnostic biomarkers has yet to be achieved. This study sought to examine the potential role of serum microRNAs (miRNAs) as biomarkers for the diagnosis of AM. Initial high-throughput Solexa sequencing revealed a significant increase in serum concentrations of miR-101-3p and miR-143-3p in patients with AM compared to healthy individuals. The results were later validated through the application of absolute quantitative reverse transcription polymerase chain reaction (qRT-PCR). Each miRNA demonstrated strong diagnostic potential, as indicated by the areas under the receiver operating characteristic (ROC) curve (AUCs) of 0.881 and 0.901, respectively. The diagnostic performance exhibited notable improvement when the two miRNAs were integrated into a panel, resulting in an AUC of 0.941. At a specific threshold of 0.385, the panel demonstrated sensitivity and specificity rates of 93.33 % and 96.67 %, respectively. Additionally, the panel demonstrated excellent discriminatory power (AUC > 0.9) in distinguishing AM from other gynecological conditions. Notably, serum miRNA levels and the composite panel score exhibited significant positive correlations with key clinical features of AM. Methodological assessments indicated that serum miRNAs remained stable under extended storage at 4 °C and after repeated freeze-thaw cycles. These results support the serum 2-miRNA panel as a reliable, non-invasive diagnostic tool for AM, with potential to enhance diagnostic precision and improve disease management.

Ethnopharmacological relevance Wenshen Xiaozheng Tang (WXT), a traditional Chinese medicine (TCM) decoction, is effective for treating endometriosis. However, the effect of WXT on endometrium-derived mesenchymal stem cells (eMSCs) which play a key role in the fibrogenesis of endometriosis requires further elucidation. Aims of the study The aim of this study was to clarify the potential mechanism of WXT in improving fibrosis in endometriosis by investigating the regulation of WXT on differentiation and paracrine of eMSCs. Materials and methods The nude mice with endometriosis were randomly divided into model group, WXT group and mifepristone group. After 21 days of treatment, the lesion volume was calculated. Fibrosis in the lesions was evaluated by Masson staining and expression of fibrotic proteins. The differentiation of eMSCs in vivo was explored using a fate-tracking experiment. To further clarify the regulation of WXT on eMSCs, primary eMSCs from the ectopic lesions of endometriosis patients were isolated and characterized. The effect of WXT on the proliferation and differentiation of ectopic eMSCs was examined. To evaluate the role of WXT on the paracrine activity of ectopic eMSCs, the conditioned medium (CM) from ectopic eMSCs pretreated with WXT was collected and applied to treat ectopic endometrial stromal cells (ESCs), after which the expression of fibrotic proteins in ectopic ESCs was assessed. In addition, transcriptome sequencing was used to investigate the regulatory mechanism of WXT on ectopic eMSCs, and western blot and ELISA were employed to determine the key mediator. Results WXT impeded the growth of ectopic lesions in nude mice with endometriosis and reduced collagen deposition and the expression of fibrotic proteins fibronectin, collagen I, α-SMA and CTGF in the endometriotic lesions. The fate-tracking experiment showed that WXT prevented human eMSCs from differentiating into myofibroblasts in the nude mice. We successfully isolated eMSCs from the lesions of patients with endometriosis and demonstrated that WXT suppressed proliferation and myofibroblast differentiation of ectopic eMSCs. Moreover, the expression of α-SMA, collagen I, fibronectin and CTGF in ectopic ESCs was significantly down-regulated by the CM of ectopic MSCs pretreated with WXT. Combining the results of RNA sequencing, western blot and ELISA, we found that WXT not only reduced thrombospondin 4 expression in ectopic eMSCs, but also decreased thrombospondin 4 secretion from ectopic eMSCs. Thrombospondin 4 concentration-dependently upregulated the expression of collagen I, fibronectin, α-SMA and CTGF in ectopic ESCs, indicating that thrombospondin 4 was a key mediator of WXT in inhibiting the fibrotic process in endometriosis. Conclusion WXT improved fibrosis in endometriosis by regulating differentiation and paracrine signaling of eMSCs. Thrombospondin 4, whose release from ectopic eMSCs is inhibited by WXT, may be a potential target for the treatment of endometriosis.

This study aimed to establish a protocol for efficiently isolating and expanding adenomyotic lesion-derived endometrial mesenchymal stem cells (A-eMSCs) in vitro. Three different methods—namely, the enzymatic method, the explant method, and the enzymatic explant method—were employed to isolate A-eMSCs. The isolation and expansion efficiencies of these three methods were subsequently compared. The enzymatic explant method was then used, and the transforming growth factor beta type I receptor (TGF-βR1) inhibitor A83-01 was added to the culture medium to evaluate its impact on the isolation and expansion efficiencies of A-eMSCs. The enzymatic explant method resulted in improved morphology, shorter cell confluence time, and greater SUSD2 enrichment in the isolation of primary endometrial cells compared to the other two methods. The proliferation and differentiation potential of A-eMSCs obtained by sorting primary endometrial cells via the enzymatic explant method were significantly higher than those obtained via the other two methods in vitro. Using the enzymatic explant method, culture medium containing A83-01 further reduced the confluence time of the cells and increased A-eMSCs enrichment during the primary endometrial cell isolation stage. Furthermore, A83-01 enhanced the proliferation and maintained the differentiation potential of A-eMSCs during the cell expansion stage. Our study identified a robust, cost-effective, and efficient protocol for isolating and expanding A-eMSCs and providing an important foundation for further research on the pathogenesis and clinical treatment of AM.

Adenomyosis (AM) is a common gynecological disorder characterized by the presence of endometrial glands and stroma within the uterine myometrium. It is associated with abnormal uterine bleeding (AUB), dysmenorrhea, and infertility. Although several mechanisms have been proposed to elucidate AM, the exact cause and development of the condition remain unclear. Recent studies have highlighted the significance of macrophage polarization in the microenvironment, which plays a crucial role in AM initiation and progression. However, a comprehensive review regarding the role and regulatory mechanism of macrophage polarization in AM is currently lacking. Therefore, this review aims to summarize the phenotype and function of macrophage polarization and the phenomenon of the polarization of adenomyosis-associated macrophages (AAMs). It also elaborates on the role and regulatory mechanism of AAM polarization in invasion/migration, fibrosis, angiogenesis, dysmenorrhea, and infertility. Furthermore, this review explores the underlying molecular mechanisms of AAM polarization and suggests future research directions. In conclusion, this review provides a new perspective on understanding the pathogenesis of AM and provides a theoretical foundation for developing targeted drugs through the regulation of AAM polarization.

OBJECTIVE:To investigate the mechanism of Bushen Huoxue decoction (, BSHXD) to treat endometriosis-induced infertility. MEDHODS:The main compounds of BSHXD were determined by high performance liquid chromatography-mass spectrometry (HPLC-MS/MS). The effect of BSHXD on Homeobox A10 (HOXA10) and alpha(v)beta(3) (αvβ3) integrin expression of Ishikawa cells, mouse model, and endometriosis-associated infertility women was evaluated by using Western blot analysis, immunohistochemistry and Real-Time quantitative polymerase chain reaction (RT-qPCR). The efficacy of BSHXD on embryo attachment were examined by using the BeWo spheroid and mouse embryo attachment assay. HOXA10 concentration in uterine flushing fluid of endometriosis-associated infertility women treated with BSHXD was measured by Enzyme-Linked immunosorbent assay (ELISA). RESULTS:BSHXD improved BeWo spheroid and mice blastocysts attachment to Ishikawa cells and increased embryo implantation rates in mice and pregnancy rates in women with endometriosis-associated infertility. BSHXD enhanced HOXA10 and αvβ3 integrin expression in Ishikawa cell, endometriosis mouse model, and endometriosis-associated infertility women, which potentially improved endometrial receptivity. CONCLUSIONS:BSHXD could improve endometrial receptivity of endometriosis-associated infertility in a dose-dependent manner by regulating HOXA10 and αvβ3 integrin expression.

Endometriosis（EMT） is a common clinical disease, and its pathogenesis is still unclear.Oxidative stress is one of the possible pathogenesis of EMT. Chinese medicinal with antioxidant effect can play the role through multiple-targets and multiple-ways, which are safe and effective with less side effects, so they are good substitutes and supplements for targeted drugs of Western medicine. This study found that TCM antioxidant therapy could effectively reduce the lesion volume, inhibit the adhesion, invasion and angiogenesis of ectopic endometrium, and curb the disease progress of EMT by regulating hormone levels and improving immunity, after sorting out the clinical and basic experimental studies on the treatment of EMT with TCM antioxidant therapy. It was found that TCM antioxidant therapy can obviously improve the clinical accompanying symptoms including pelvic pain and infertility related to EMT, and effectively delay the deterioration of EMT. Therefore, TCM antioxidant therapy is a potential therapy that can not only inhibit the progress of EMT, but also alleviate the associated symptoms of EMT, so as to provide new ideas for clinical treatment of the disease.

Tumor cell extravasation across endothelial barrier has been recognized as a pivotal event in orchestrating metastasis formation. This event is initiated by the interactions of extravasating tumor cells with endothelial cells (ECs). Therefore, targeting the crosstalk between tumor cells and ECs might be a promising therapeutic strategy to prevent metastasis. In this study, we demonstrated that Rh1, one of the main ingredients of ginseng, hindered the invasion of breast cancer (BC) cells as well as diminished the permeability of ECs both in vitro and in vivo, which was responsible for the attenuated tumor cell extravasation across endothelium. Noteworthily, we showed that ECs were capable of inducing the epithelial-mesenchymal transition (EMT) and invadopodia of BC cells that are essential for tumor cell migration and invasion through limiting the nuclear translocation of hematopoietically expressed homeobox (HHEX). The decreased nuclear HHEX paved the way for initiating the CCL20/CCR6 signaling axis, which in turn contributed to damaged endothelial junctions, uncovering a new crosstalk mode between tumor cells and ECs. Intriguingly, Rh1 inhibited the kinase activity of casein kinase II subunit alpha (CK2α) and further promoted the nuclear translocation of HHEX in the BC cells, which resulted in the disrupted crosstalk between chemokine (C-C motif) ligand 20 (CCL20) in the BC cells and chemokine (C-C motif) receptor 6 (CCR6) in the ECs. The prohibited CCL20-CCR6 axis by Rh1 enhanced vascular integrity and diminished tumor cell motility. Taken together, our data suggest that Rh1 serves as an effective natural CK2α inhibitor that can be further optimized to be a therapeutic agent for reducing tumor cell extravasation.

目的 探讨止带汤加减联合宫颈敷料对宫颈LEEP术后创面愈合的临床疗效.方法 将180例宫颈上皮内瘤变患者随机分为对照组(62例)、宫颈敷料组(66例)和联合治疗组(52例).对照组采用常规方法进行换药,宫颈敷料组在对照组基础上加用宫颈敷料,联合治疗组在宫颈敷料组基础上加服止带汤加减4周.观察阴道流血、排液,创面愈合、感染、出血以及宫颈管粘连等情况.结果 3组均未见术后创面感染.与对照组相比,宫颈敷料组和联合治疗组的阴道流血、排液及创面愈合时间明显缩短(P＜0.05);联合治疗组阴道排液、创面愈合时间显著短于宫颈敷料组(P＜0.01).宫颈敷料组和联合治疗组的术后并发症发生率低于对照组(P＜0.05);其中,联合治疗组的术后并发症发生率较宫颈敷料组显著降低(P＜0.01).结论 止带汤加减联合宫颈敷料有助于宫颈上皮内瘤变患者LEEP术后创面愈合,避免术后并发症发生,有临床推广应用价值.

子宫内膜异位症(EMs)影响女性生殖系统,越来越多的具有生育要求的EMs女性生育力下降.泛素化是蛋白质翻译后修饰的方式之一,在妇科疾病中,泛素化调控了多种关于EMs相关的信号通路,并在肿瘤增殖和移植中发挥了很多作用.S相激酶相关蛋白2(SKP2)是参与泛素化的一种蛋白,在生殖中至关重要.在EMs不孕中,SKP2通过泛素化同源框基因A10(HOXA10),降低子宫内膜容受性.由此提示治疗的新选择可以通过抑制SKP2泛素化HOXA10,从而改善子宫内膜容受性,提高妊娠率.本文通过查阅国内外的相关文献报道,阐述泛素化和EMs不孕的相关性研究,为EMs不孕患者提供新的治疗方案.

子宫内膜异位症(EMs)是育龄期妇女的常见病、多发病,目前其发病机制尚不明确.因具有激素依赖性、侵袭强和复发率高等特点,在临床诊疗过程中有一定的难度和挑战.近年来旁分泌成为EMs的研究热点.旁分泌效应产生的各种生物活性分子和外泌体参与EMs的形成,具体可能通过介导炎症与免疫反应,促细胞增殖与抑制凋亡,促血管新生,分化或转化,细胞外基质的合成等途径参与EMs的发生发展.本文综述了近年来常见的旁分泌因子及外泌体在EMs发病机制中的作用及研究进展,为EMs的防治提供新的切入点.

This study aimed to identify differentially expressed genes (DEGs) and molecular pathways in eutopic endometrial stromal cells (EuESCs) from adenomyosis (AM) patients and to provide a new insight into the disease mechanisms. The gene expression profiles in adenomyotic EuESCs (A-EuESCs) and normal ESCs (N-ESCs) were analyzed by RNA-sequencing (RNA-Seq) and validated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways enrichment analyses were performed to obtain insights into the functions of DEGs. The protein-protein interaction (PPI) network was constructed using the STRING database and visualized by Cytoscape software, and their hub genes were identified. A total of 458 up-/363 down-regulated genes were identified in A-EuESCs versus N-ESCs. The GO enrichment analysis showed that these genes were significantly enriched in calcium-dependent cell-cell adhesion. The most significant term of the KEGG pathway analysis was cytokine-cytokine receptor interaction. There were 145 nodes in the PPI network of the 157 DEGs, which were identified in significant enrichment pathway by the KEGG pathway analysis in N-ESCs and A-EuESCs. The PPI network revealed that IL-6 was a central hub gene. Besides, IL-6 was found as a central hub gene in the pro-inflammatory/chemotactic subnetwork, and EGF was noted as a central hub gene in the angiogenesis subnetwork. Our study indicated the alterations of transcriptomic profiles in A-EuESCs and provided new insights into the pathogenesis of AM. The A-EuESCs in women with AM have fundamental abnormalities that may predispose to pro-invasion/migration and angiogenesis.

目的 研究宫颈高危型人乳头状瘤病毒(HR?HPV)感染中医证型、体质分布及相关危险因素,为中医药防治提供临床依据.方法 通过流行病学调查分析宫颈HR?HPV感染患者的中医证型、体质及两者相关性,多因素logistic回归分析宫颈HR?HPV感染相关危险因素.结果 本研究共调查782例,其中宫颈HR?HPV感染309例,总体感染率为39.51％;不同年龄段的感染率分布大致呈"U"形.感染人群多见脾虚湿热证(50.48％,156/309),体质分布以湿热质(25.89％,80/309)、阳虚质(17.48％,54/309)为主;部分体质与中医证型联系紧密.多因素回归结果显示,年龄20～39岁、多孕多产和湿热质体质为宫颈HR?HPV感染独立危险因素(Ρ<0.05),平和质体质是保护因素(Ρ<0.05).结论 宫颈HR?HPV感染受到多因素的影响,临床工作中应做到体、病、证三位一体,及早针对相关危险因素采取干预措施,以达到未病先防、既病防变、预后防复的效果.

白细胞介素-33(IL-33)作为白细胞介素-1细胞因子超家族的新成员,在各种疼痛反应过程中发挥调节作用.通过回顾炎症性疼痛、神经性疼痛、骨癌痛、手臂振动综合征、疼痛性膀胱综合征以及急性心肌梗死等疾病文献中的IL-33含量,发现IL-33在不同组织、系统中存在表达差异,且IL-33可诱导生长刺激表达基因2蛋白(ST2)受体广泛表达(尤其是辅助性T2细胞和肥大细胞),以核因子κB(NF-κB)依赖的方式产生促炎性物质,释放信号因子,促进下游通路中炎症反应的发生,进而参与T细胞介导的免疫应答,这为疼痛的治疗提供了新思路.

子宫内膜异位症常发生于已婚育龄妇女,发病率为5％～10％.其临床症状为不同形式的疼痛,而目前对于其疼痛的发生机制了解较少,主要和神经生长因子、神经纤维、炎症反应等相关.对子宫内膜异位症所致疼痛患者进行针对性的治疗和护理有助于提升其生活质量.目前的治疗方式主要有手术、药物、中医治疗,但都存在一定程度的局限性,包括反复发作、副作用、费用高等.因此,有必要对子宫内膜异位症发病机制、治疗方式进行更深层次的研究,以期找到并制定更优化的治疗方案,为患者减轻痛苦.本文通过查阅国内外的相关文献报道,特对子宫内膜异位症致疼痛的发生机制及其治疗措施进行了综述,希望可以为相关医护人员及患者提供参考,改善子宫内膜异位症致疼痛患者的疼痛状况.

多囊卵巢综合征(PCOS)好发于育龄期妇女,以月经失调、不孕等为主要临床表现,发病率逐年升高.目前西医治疗以降低雄激素、改善胰岛素抵抗、促排卵为主,但有一定的局限性,包括疗效欠佳、并发症多等.多项研究发现,PCOS发生发展与肠道菌群相关.肠道菌群被称为"人类第二大基因组""被遗忘的器官",近年来成为感染性、免疫性以及代谢性疾病的研究热点.本文主要从肠道菌群失调所致的高雄激素血症、胰岛素抵抗、慢性炎症及代谢综合征探讨与PCOS发生和发展的相关性.中医运用中药复方、针灸等方式调和胃肠肝脾、平衡肠道菌群、维持肠道内环境稳态,为PCOS病因病机的认识及治疗提供新的切入点.