Due to the lack of classic estrogen receptors, there has been a shortage of targeted therapy for triple-negative breast cancer (TNBC), resulting in a poor prognosis. However, the newly discovered G protein-coupled estrogen receptor (GPER) has been found to be expressed in TNBC cells. Salvia miltiorrhiza (Danshen) is an essential Chinese medicine for gynecological disorders, and its component tanshinone IIA (Tan IIA) exerts an anticancer effect. Therefore, this study attempted to investigate whether GPER is involved in the inhibitory effect of Tan IIA on TNBC. We applied various databases and GO pathway analysis to predict the possible mechanism of Tan IIA. We identified 39 overlapping targets, including c-Jun, c-Fos, and caspase-3, and enriched cell cycle-related pathways. Next, we demonstrated the strong binding ability of Tan IIA to GPER by molecular docking assay. In the subsequent validation tests, Cell Counting Kit-8 (CCK8) assay showed that Tan IIA inhibited proliferation of MDA-MB-231 cells time and dose dependently without affecting normal cells. Using Transwell plate, flow cytometry, and Western blot assays, we showed that Tan IIA inhibited migration and induced apoptosis of MDA-MB-231 dose dependently. Importantly, protein expressions of GPER, epidermal growth factor receptor (EGFR), extracellular regulated protein kinases (ERK), c-Fos, and c-Jun were all decreased by Tan IIA dose dependently. Administration of GPER inhibitor partly abolished these effects. Furthermore, nuclear translocation of c-Fos and c-Jun as well as cell cycle-related proteins was downregulated by Tan IIA dose dependently. In summary, Tan IIA could inhibit the proliferation and migration of MDA-MB-231 cells and induce apoptosis, and the possible mechanism may be the regulation of GPER-mediated pathways, suggesting that GPER could be a therapeutic target for TNBC.

乳腺癌的转移是其临床治疗面临的重点和难点,其侵袭性的高低受周围基质的影响很大.癌症相关成纤维细胞(CAFs)是肿瘤基质的重要成分,同时也是新型膜雌激素受体——G蛋白耦联雌激素受体(GPER)阳性细胞.研究表明,GPER可能是作用于癌细胞与肿瘤微环境(TM)的多种重要传导因子之间的关键交叉点,GPER在CAFs中活化对乳腺癌发生、发展和转移过程中发挥着重要的作用.多种中药单体的抗乳腺癌作用也与其靶向激活CAFs中的GPER通路是相关的.现就GPER在CAFs中的活化机制及其对乳腺癌转移的作用、中药单体对该过程的干预研究进行综述,以期为寻找乳腺癌治疗的新靶点、拓展乳腺癌症治疗策略提供思路.

目的:通过观察小檗碱(BBR)对卵巢颗粒细胞衰老的影响,探究其保护作用及调节机制.方法:应用H2O2诱导建立人卵巢颗粒样肿瘤(KGN)细胞衰老模型;设置空白组、模型组、BBR高剂量(1 μmol·L-1)组和BBR低剂量(0.5 μmol·L-1)组,模型组与BBR组加入浓度为10 μmol·L-1H2O2,孵育40 min.通过细胞增殖与活性检测(CCK-8)分析检测BBR对KGN细胞增殖的影响;通过β-半乳糖苷酶染色检测BBR对KGN细胞衰老状态的影响;应用流式细胞术检测BBR对KGN细胞凋亡和ROS含量的影响;实时荧光定量聚合酶链式反应(Real-time PCR)检测BBR对KGN细胞抗凋亡蛋白B细胞淋巴瘤-2(Bcl-2)/促凋亡蛋白Bcl-2相关X蛋白(Bax)比值、胱天蛋白酶-3(Caspase-3)、叉头框转录因子O1(FoxO1)及过氧化氢酶(CAT)mRNA表达的影响;蛋白免疫印迹法(Western blot)检测BBR对KGN细胞沉默信息调节因子1(SIRT1)、超氧化物歧化酶2(SOD2)、c-Jun氨基末端激酶(JNK)、FoxO1、自噬相关蛋白微管相关蛋白轻链3Ⅱ(LC3BⅡ)、自噬关键分子酵母Atg6(Beclin-1)及泛素结合蛋白p62蛋白表达的影响.结果:H2O2诱导40 min后,与空白组比较,模型组细胞增殖率显著下降(P＜0.01);与模型组比较,BBR干预组细胞增殖率明显上升(P＜0.05);β-半乳糖苷酶染色结果显示,与空白组比较,模型组细胞呈现明显的衰老状态(P＜0.01),BBR干预组细胞衰老情况较模型组显著降低(P＜0.01);流式细胞术检测显示,与空白组比较,模型组细胞凋亡率显著上升(P＜0.01),BBR干预组细胞凋亡率较模型组明显降低(P＜0.05);同时,与空白组比较,模型组ROS含量显著增加(P＜0.01);与模型组比较,BBR干预组细胞ROS含量显著降低(P＜0.01);Real-time PCR结果显示,与空白组比较,模型组KGN细胞CAT、Bcl-2/Bax mRNA表达明显降低,Caspase-3与FoxO1 mRNA表达明显增加(P＜0.05);与模型组比较,BBR干预后KGN细胞CAT与Bcl-2/Bax mRNA表达明显增加(P＜0.05),Caspase-3与FoxO 1 mRNA表达较模型组明显降低(P＜0.05).Western blot结果显示,与空白组比较,模型组SIRT1、SOD2及p62蛋白水平显著降低(P＜0.01),JNK、FoxO1、LC3B Ⅱ与Beclin-1蛋白水平明显升高(P＜0.05);BBR干预后,SIRT1、SOD2及p62蛋白水平较模型组显著增加(P＜0.01),JNK、FoxO1、LC3BⅡ与Beclin-1蛋白水平较模型组明显降低(P＜0.05).结论:BBR具有抑制卵巢颗粒细胞衰老效应,其机制与通过SIRT1/FoxO1通路介导抑制细胞凋亡与自噬有关.

Ethnopharmacological relevant: Erxian Decoction (EXD) has been used empirically for more than 70 years to treat premature ovarian failure (POF), but more research is needed to understand how it works.Aim of the research: The study aims to ascertain both in vivo and in vitro rewards of EXD.Materials and methods: EXD is composed of Curculiginis Rhizoma, Epimedii Folium, Morindae Officinalis, Angelicae Sinensis, Anemarrhenae Rhizoma, and Phellodendri Chinensis Cortex. UPLC/MS analysis was used to investigate the components of EXD. Using a POF model created by administering cisplatin to rats intraperitoneally, the pharmacodynamic effects of EXD were investigated. Three dose groups of EXD were garaged into rats: high (15.6 g/kg), medium (7.8 g/kg), and low (3.9 g/kg). By using a vaginal smear, the impact of EXD on the rat estrous cycle was evaluated. An ELISA test was used to measure the anti-Mullerian hormone (AMH), estradiol (E2), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) levels in the serum of rats. By using HE stains, pathological alterations in the ovaries may be seen. MDA and SOD levels in ovarian samples were used to measure the degree of ovarian oxidation. TUNEL labeling of ovarian sections was used to find apoptosis levels. By using ATP, energy production was evaluated. The relative expression of proteins connected to aging and the RAGE pathway was assessed using Western blot. Then, using H2O2, a model of senescent human ovarian granulosa cells (KGN) was created in vitro. The impact of EXD and H2O2 on cellular senescence was discovered using-galactosidase staining. Cell apoptosis levels were found using PI/Hoechest33342. By using DCFH-DA, intracellular ROS was examined. MDA and SOD concentrations were used to measure the degree of cellular oxidation. RAGE-related mRNA and protein expression were evaluated using RT-qPCR and western blotting.Results: Using UPLC/MS analysis, 39 chemicals in EXD were found. Rats' estrous cycles were enhanced by EXD, which increased ovarian index and follicle count and reduced the proportion of atretic follicles in the rats. EXD reduced LH and FSH output while restoring AMH and E2 secretion. In ovarian tissues, EXD reduced the amount of apoptosis and MDA while raising SOD activity and ATP levels. The protein levels of p16, p21, p53, and Lamin A/C were among the senescence-related proteins that EXD lowered, along with the levels of RAGE, PI3K, BAX, and CASPASE 3. Anti-apoptotic protein BCL-2 was also raised in the RAGE pathway. Senescence, apoptosis, ROS, and MDA levels in the KGN cells were lowered in vitro by EXD. Additionally, EXD increased the anti-apoptotic potential by changing the expression of CAT, SOD2, and SIRT1. RAGE, BAX, BCL-2, CASPASE 3, and p38 expression levels were altered by EXD, enhancing its anti-apoptotic capability.Conclusion: EXD boosted the ovary's antioxidant and anti-apoptotic capabilities while enhancing the estrous cycle and hormone output. These findings strongly suggested that EXD may contribute to the alleviation of POF and ovarian granulosa cells senescence.

目的:探讨四物汤通过胰岛素样生长因子-1(Insulin-ike growth factors-1,IGF-1)/磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(AKT)/雷帕霉素靶蛋白(Mammalian target of rapamycin,mTOR)mTOR信号通路发挥对4-乙烯基环己烯二环氧化合物(4-Vinylcyclohexene Diepoxide,VCD)诱导的卵巢衰老大鼠骨骼肌的保护作用及其分子机制.方法:选用28日龄雌性F-344大鼠,随机选取6只作为空白对照组,剩余大鼠连续腹腔注射VCD溶液(160mg/kg/d)20天,每天阴道涂片检测动情周期,连续观察12 d无角化细胞或仅有少量角化细胞即符合"卵巢衰老"表现,经动情周期筛选出24只造模成功的大鼠,分为模型组(Model)、阳性(戊酸雌二醇,E2)对照组、四物汤高剂量(SWT-H)组和四物汤低剂量(SWT-L)组,每组6只,灌胃持续3周后取材.取大鼠骨骼肌组织进行HE染色观察病理组织结构;MASSON染色骨骼肌纤维形态变化;RT-PCR检测骨骼肌组织中各基因的mRNA水平.结果:与空白组比较,模型组骨骼肌肌纤维排列疏松,分布不均且有断点,胞浆不均,细胞核增多,出现增生的结缔组织,胶原纤维逐渐增多且肌纤维间距变宽;与模型组相比,E2组、SWT-H组与SWT-L组肌纤维排列相对整齐,胞浆较为均匀.肌肉形态较规则,纤维间距缩短,胶原纤维减少.RT-PCR结果显示,与空白组相比,模型组IGF-1、PI3K、AKT、mTOR基因的mRNA表达量明显下调,E2组、SWT-H组与SWT-L组的IGF-1、PI3K、mTOR的表达明显上升,SWT-H组AKT表达无明显变化,无统计学意义,SWT-L组AKT表达相对降低.与模型组相比,E2组、SWT-H组与SWT-L组的IGF-1、AKT、mTOR的表达明显增加,且具有剂量依赖性,PI3K表达增加,但无明显剂量依赖性.结论:四物汤可以明显改善VCD诱导的卵巢衰老大鼠的肌肉减少情况,其机制可能是通过IGF-1-PI3K-AKT-mTOR信号通路来发挥其抑制肌肉流失的作用.

目的:基于体外细胞实验,探索丹参酮ⅡA对三阴性乳腺癌细胞MDA-MB-231迁移的抑制作用及其分子机制.方法:选取三阴性乳腺癌细胞MDA-MB-231,利用细胞增殖实验检测丹参酮Ⅱ A对MDA-MB-231细胞增殖的作用,并筛选适宜的药物浓度;应用划痕实验检测丹参酮ⅡA对MDA-MB-231细胞迁移率的影响;Western Blot法检测丹参酮Ⅱ A对G蛋白偶联雌激素受体(G protein-coupled estrogen receptor,GPER)及基质金属蛋白酶 9(Matrix metalloprotein-9,MMP-9)表达的影响.结果:细胞增殖实验结果显示,丹参酮ⅡA可以抑制MDA-MB-231细胞增殖,且呈剂量依赖性(P＜0.05);划痕实验结果显示,丹参酮Ⅱ A可以抑制MDA-MB-231细胞迁移,且呈剂量依赖性(P＜0.01),加入GPER特异性抑制剂G15后迁移率有所上升(P＜0.01).Western Blot结果显示,丹参酮ⅡA可以显著下调GPER和MMP-9蛋白的表达水平并呈剂量依赖性(P＜0.05),加入GPER特异性抑制剂G15后,MMP-9表达有所上升(P＜0.01).结论:丹参酮Ⅱ A可以抑制三阴性乳腺癌细胞MDA-MB-231迁移,其机制可能与抑制GPER介导的MMP-9表达相关.

This study explored the phytoestrogen-like effect of Siwu Decoction(SWD) and the estrogen receptor(ER)-mediated molecular mechanism based on network pharmacology and in vivo experiment. The active components and targets of SWD were retrieved from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform(TCMSP), and related targets of "estrogen" from GeneCards and Online Mendelian Inheritance in Man(OMIM). Cytoscape and STRING were employed to construct the protein-protein interaction(PPI) network and "chemical component-target-disease" network and core targets were identified, followed by Gene Ontology(GO) term enrichment and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment of the core targets by R software. For the in vivo experiment, the 22-day-old SD female rats were treated(ig) with SWD for 4 days. Via hematoxylin-eosin(HE) staining, the morphological changes of rat uterus were observed. Reverse transcriptase-polymerase chain reaction(RT-PCR) was performed to detect mRNA expression of ER subtypes, estrogen-related targets, and the main regulatory factors in the estrogen signaling pathway. The results indicated 74 targets of SWD exerted phytoestrogen-like effect. KEGG pathway enrichment result suggested that estrogen signaling pathway was closely related to the phytoestrogen-like effect of SWD. Rats in SWD group demonstrated significantly thickened endometrium and significantly decreased expression of ERα, ERβ, and G protein-coupled estrogen receptor(GPER) mRNA in ovarian tissue. In addition, significant lowering of ERα and ERβ mRNA expression and significant rise of GPER mRNA expression in uterine tissue were observed in the SWD group. The expression of mitogen-activated protein kinase(MAPK) p38, MEK1/2 and extracellular signal-regulated kinase(ERK)1/2 mRNA was significantly low while that of epidermal growth factor receptor(EGFR) mRNA was significantly high in both ovarian and uterine tissues of SWD group compared with those in the control group. In conclusion, the phytoestrogen-like effect of SWD is closely related to the estrogen signaling pathway. The result lays a basis for revealing molecular mechanism of SWD in the treatment of gynecological diseases.

目的 探究人参皂苷Rg1对顺铂损伤大鼠卵巢颗粒细胞的保护作用及分子机制.方法 选取22～24 d SD的大鼠提取卵巢颗粒细胞进行原代培养,应用顺铂诱导建立卵巢早衰模型.设置正常组,模型组,人参皂苷Rg1低浓度组、中浓度组、高浓度组和雌二醇(E2)组.HE染色及免疫细胞化学法进行颗粒细胞鉴定;CCK8法检测人参皂苷Rg1作用24 h、48 h对顺铂损伤颗粒细胞的保护作用;Hoechst 33258染色检测细胞凋亡;Western blot法检测FSHR、PI3K、p-AKT、AKT、Bcl-2和Bax的蛋白表达.结果 细胞形态观察和胞质FSHR表达检测结果均表明所提取细胞为卵巢颗粒细胞;顺铂处理12h后,颗粒细胞增殖率呈剂量依赖性下降,而给予人参皂苷Rg1后,细胞增殖率下降被显著抑制,且呈剂量和时间依赖性;与模型组比较,人参皂苷Rg1和E2处理后卵巢颗粒细胞中FSHR、PI3K、p-AKT/AKT及Bcl-2/Bax蛋白表达水平显著上升,而PI3K抑制剂干预后,Bcl-2蛋白表达显著下降.结论 人参皂苷Rg1对顺铂损伤的卵巢颗粒细胞具有保护作用,该保护作用可能通过激活FSHR/PI3K/AKT通路,抑制卵巢颗粒细胞凋亡实现.

Abstract Background Bone protective effect of Si-Wu-Tang (SWT), a classical prescription of traditional Chinese medicine, is verified in clinical for thousand years. However, its mechanisms were still unclear. This study aims to investigate the molecular mechanism in ApoE -/- mice fed a high-fat diet combining network pharmacology and in-vivo experiments. Methods Femurs were collected from 6 ~ 8-week-old female ApoE-/- C57BL/6J mice (n = 12, 18–22 g) and their age-matched wild-type (WT) littermates C57BL/6J mice (n = 6, 18–20 g). They were divided into 3 groups: the control, SWT and model groups. Serum levels of high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) were measured by the serum biochemical index. HE staining and immunohistochemistry analysis were performed to observe the pathological tissue structure and the location and expression level of targets from the pathway screened out by the network pharmacology method. Western blot (WB) and RT-PCR analyses were performed to detect the expression levels of target proteins and mRNAs, respectively. Results The results of the network pharmacology analysis showed that the mechanism of SWT in treating osteopenia was closely related to the oestrogen receptor (ER) signalling pathway. In vivo experiments indicated that, compared with control group, the distribution of bone trabeculae was sparse, and the bone density decreased. The levels of HDL-C and LDL- C in the serum of the model group increased significantly (p < 0.01). The expression of GPER, PI3K, AKT and BCL-2 in the bone tissue of the model group decreased, and P53, BAX, ERα and ERβ were upregulated. Compared with the model group, the body mass of the SWT group increased slowly. The bone density and the distributions of bone trabeculae both increased. The expression of ERα, ERβ, GPER, PI3K, AKT and BCL-2 increased. The decreased expression of apoptotic genes, including P53 and BAX, was observed. Conclusion SWT significantly reduced bone loss in ApoE -/- mice fed a high-fat diet. An important mechanism might be that SWT could activate the PI3K/AKT signalling pathway mediated by ER and then inhibit apoptosis-related proteins to exert bone protective effects.

G protein-coupled estrogen receptor (GPER) was reported to be a potential target in the breast cancer therapy. This study aimed to illuminate the function of GPER and its mediated PI3K/AKT pathway in cryptotanshinone (CPT) inducing cell apoptosis and antiproliferation effect on GPER positive breast cancer MCF-7 cells. Cell proliferation was tested by MTT assay. Apoptosis rates were tested by Annexin V-FITC/PI double staining and the cell cycle was researched by flow cytometry. Autodock vina was applied to make molecular docking between CPT or estradiol and GPER. siRNA technique and GPER specific agonist G-1 or antagonist G-15 were applied to verify the mediated function of GPER. Apoptosis and cell cycle related proteins, as well as the key proteins on PI3K/AKT signaling pathway were detected by western blot. The results indicated that CPT could exert antiproliferation effects by arresting cell cycle in G2/M phase and downregulating the expression of cyclin D, cyclin B and cyclin A. Besides, apoptosis induced by CPT was observed. CPT might be a novel GPER binding compounds. Significantly, suppression of PI3K/AKT signal transduction by CPT was further increased by G-1 and decreased by G-15. The study revealed that the effect of antiproliferation and apoptosis treating with CPT on MCF-7 cells might be through the downregulation of PI3K/AKT pathway mediated by activated GPER.

四物汤的应用从古至今已有悠久的历史,原为外伤"重伤肠内有淤血者"而设,后世多用于治疗血虚血滞等疾病.对于这一补血调经的良方,国内外学者进行了广泛而深入的研究,发现四物汤及组方中药的有效成分具有补血、调经、雌激素样作用、抗氧化、改善脑损伤、抗癌等多种药理作用,并且在妇科、骨科等临床方面的疗效较为显著.本文对近年来的研究成果进行了梳理和总结,将四物汤的药理作用和临床应用进行综述,以期为四物汤的深入研究提供理论依据,为临床用药提供参考.

Ethnopharmacological relevance: Si-Wu-Tang (SWT), a prestigious herbal formula from China, has been extensively used for centuries for female-related diseases. It has been documented that SWT has a significant inhibitory effect on non-triple-negative breast cancer (non-TNBC) cells. However, there has been limited comprehensive analysis of the targeted effects of the anticancer components of SWT and its exact biological mechanism. Aim of the study: This study aims to uncover the mechanism by which SWT treats non-TNBC by applying a network pharmacological method combined with experimental validation. Materials and methods: First, SWT compounds were collected from the Traditional Chinese Medicines Systems Pharmacology database (TCMSP) and The Encyclopedia of Traditional Chinese Medicine (ETCM), and then the targets related to SWT were obtained from the TCMSP and SwissTarget databases. Second, a target data set of non-TNBC proteins was established by using the Online Mendelian Inheritance in Man (OMIM), GeneCards and Gene Expression Omnibus (GEO) databases. Third, based on the overlap of targets between SWT and non-TNBC, a protein-protein interaction (PPI) network was built to analyse the interactions among these targets, which focused on screening for hub targets by topology. On these hub genes, we conducted a meta-analysis and survival analysis to screen the best match targets, ESR1, PPARG, CAT, and PTGS2, which had a strong correlation with the ingredients of SWT in our verification by molecular docking. In vitro experiments further proved the reliability of the network pharmacology findings. Finally, FunRich software and the ClusterProfiler package were utilized for the enrichment analysis of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) data. Results: A total of 141 active ingredients and 116 targets of SWT were selected. GO enrichment analysis showed that the biological processes through which SWT acted against non-TNBC (FDR<0.01) mainly involved modulating energy metabolism and apoptosis. According to RT-qPCR and Western blotting, the mRNA and protein expression of ESR1, PPARG and PTGS2 were upregulated (P < 0.01), and the mRNA and protein levels of CAT were downregulated (P < 0.01), suggesting a multi-gene regulatory molecular mechanism of SWT against nontriple-negative breast cancer. Conclusions: This research explored the multi-gene pharmacological mechanism of action of SWT against nonTNBC through network pharmacology and in vitro experiments. The findings provide new ideas for research on the mechanism of action of Chinese medicine against breast cancer.

目的 探讨四物汤在大鼠脑和骨骼肌组织中发挥雌激素样效应的机制.方法 将20只未达性成熟雌性SD大鼠完全随机分为正常对照组、雌激素组、四物汤高剂量组和低剂量组,各5只,适应性喂养4d后,正常对照组予相等剂量0.9％氯化钠溶液灌胃,雌激素组予戊酸雌二醇0.104 mg/(kg·d)灌胃,四物汤高剂量组予四物汤2.08 g/(kg·d)灌胃,四物汤低剂量组予四物汤0.52g/(kg·d)灌胃.每日早晚各灌胃1次,连续4d.各组大鼠最后一次灌胃后3h称重,10％水合氯醛腹腔麻醉后腹主动脉快速取血处死.观察大鼠脑及腿部骨骼肌组织细胞形态,采用蛋白质印迹法检测雌激素受体β(ERβ)、G蛋白偶联雌激素受体(GPER)、磷脂酰肌醇-3-激酶(PI3K)及蛋白激酶B(Akt)表达情况.结果 4组大鼠脑和骨骼肌组织细胞形态均未出现明显变化.在脑组织中,四物汤低剂量组ERβ表达量显著低于正常对照组和雌激素组[(0.354±0.066)比(0.450±0.022)、(0.509±0.042)];四物汤高剂量组和四物汤低剂量组GPER表达量显著低于雌激素组;四物汤低剂量组PI3K表达量显著低于正常对照组[(0.255±0.086)比(0.404 ±0.100)];雌激素组和四物汤高剂量组Akt表达量显著低于正常对照组[(0.224±0.049)、(0.268±0.097)比(0.467 ±0.102)](均P＜0.05或P＜0.01).在骨骼肌组织中,雌激素组和四物汤低剂量组ERβ表达量显著低于正常对照组;四物汤低剂量组PI3K表达量显著高于正常对照组和雌激素组,Akt表达量显著低于正常对照组和雌激素组(均P＜0.05或P＜0.01).结论 四物汤可不同程度抑制脑组织中ERβ、GPER、PI3K、Akt及骨骼肌中ERβ、Akt的表达,促进骨骼肌中PI3K的表达.推断四物汤可能通过ERβ和GPER介导的PI3 K/Akt信号通路发挥雌激素样效应.

乳腺增生症是一种乳腺组织异常增生的疾病,中医学认为其发生与肝、脾、胃及冲任密切相关,且在肾气-天癸-冲任-胞宫轴的影响下呈现周期性变化.本文以月经周期中冲任气血的消长、阴阳消长变化规律和乳腺的周期性变化为理论依据,分析了乳癖的病因病机,阐明了月经周期各阶段的特点和乳癖的周期治则治法,并提出行经期是治疗乳腺增生症的关键时期,若抓住此时契机,因势利导,活血化瘀,是治疗乳腺增生症的捷径.

目的 探讨中医和西医方法联合使用治疗乳腺增生症的效果,为疾病治疗提供科学参考.方法 随机选取本院2017年2月～2018年5月收治的52例乳腺增生症患者作为研究对象,将其分为单纯西医组和中西医组.予以单纯西医组患者常规西医治疗方法,中西医组患者实行中西医结合的治疗模式.结果 中西医组患者治疗效果为92.31％,随访三个月后无复发患者,且中西医组患者的乳房肿块明显缩小,疼痛程度明显减轻.单纯西医组患者的治疗有效率不足80％,且经过三个月的随访后,有5例患者出现复发状况.结论 在乳腺增生症的治疗过程中,应在西医治疗的基础上,加用中医方法,消除患者的乳腺肿块,提升治疗效果.