|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Efficacy of Lubeikangru formulation in mice with hyperplasia of the mammary glands induced by estrogen and progesterone显示文摘OBJECTIVE: To evaluate the protective effects of Lubeikangru formula(LF) on hyperplasia of the mammary glands(HMG) induced by estrogen and progesterone in mice.METHODS: Female mice were divided randomly into five groups: normal, model, tamoxifen(3 mg/kg),Rupixiao(900 mg/kg) and LF(900 mg/kg). All mice except those in the normal group were treated sequentially with estradiol and progesterone to induce HMG. From the tenth day of induction, mice in normal and model groups received distilled water and mice in the other groups were given the corresponding drugs by gavage, once a day, for 30 d.At the end of treatment, the mammary glands, ovaries, hypothalamus, and serum was collected for whole-mount and hematoxylin and eosin(HE)staining, enzyme-linked immunosorbent assays(ELISAs), or western blotting.RESULTS: Whole-mount and HE staining of mammary glands showed that LF rescued(at least in part) the hyperplasic morphology of the mammary glands, and the number of branch points decreased after LF treatment(P < 0.05). ELISAs revealed that levels of estrogen and progesterone were decreased following LF treatment, whereas levels of gonadotropin-releasing hormone, follicle-stimulating hormone, and luteinizing hormone were increased in serum and tissues. Western blotting confirmed that LF treatment led to a reduction in expression of phosphorylated(p)-Erk, p-p38 and p-c-Jun N-terminal kinase. LF was also confirmed to be safe by acute-toxicity tests.CONCLUSION: LF can protect the mammary glands of mice from estrogen-and progesterone-induced hyperplasia by adjusting hormone levels and regulating the mitogen-activated protein kinase pathway. | Sun Li Guo Donghui Liu Qian Xue Yanan Jiang Ning Zheng Hongxin | 2019 | Journal of Traditional Chinese Medicine2019，39，2： | 8 |
| 2 | 不同子宫术式对子宫肌瘤患者性激素水平和乳腺增生症的影响显示文摘【目的】探讨不同子宫术式对子宫肌瘤患者术后性激素水平和乳腺增生症发生的影响。【方法】选择子宫肌瘤患者168例,根据不同术式分为肌瘤剔除术组(n=52,A组)、次全子宫切除术组(n=57,B组)、全子宫切除术组(n=59,C组)。比较三组患者术后乳腺增生症发生率及术前、术后3个月、术后6个月、术后1年的卵泡生成激素(FSH)、黄体生成激素(LH)、雌二醇(E2)、孕酮(P)、催乳素(PRL)水平。【结果】B组、C组乳腺增生症发生率分别为28.07%和35.09%,均显著高于A组9.62%,差异有统计学意义(P〈0.05);B组、C组术后3个月、6个月、12个月时FSU、LH水平均显著高于术前和A组,差异有统计学意义(P〈0.05);B组、C组术后3个月、术后6个月PRL水平均显著高于术前和A组,差异有统计学意义(P〈0.05);B组、C组E2水平术后3个月、6个月、12个月显著低于术前和A组,差异有统计学意义(P〈0.05)。【结论】全子宫切除术和次全子宫切除术均可使子宫肌瘤患者术后性激素水平发生异常改变,乳腺增生症发生率显著增加,而子宫肌瘤剔除术患者体内性激素水平无明显改变。 | 姜炬芳 邓五一 徐艳红 | 2016 | 医学临床研究2016，33，3： | 6 |
| 3 | External use of Ruyanneixiao cream efficiently blocks precancerous mammary lesions by interfering with glycolysis induced by inhibition of hypoxia inducible factor-1α, hexokinase 2, phosphofructokinase, and pyruvate kinase M2 expression显示文摘OBJECTIVE:To investigate the effect of Ruyanneixiao cream(RYNX) on the expression of hypoxia inducible factor-1α(HIF-1α), hexokinase 2(HK2),phosphofructokinase(PFK), and pyruvate kinase M2(PKM2) mRNA and protein in MCF-10 AT cells and in an animal model of precancerous mammary lesions.METHODS:Following treatment of MCF-10 AT cells with RYNX, tamoxifen(TAM) and YC-1 for 48 h,HIF-1α, HK2, PFK, PKM2 mRNA and protein expression was analyzed.Fifty female SD rats were randomly divided into control, model, TAM, and highand low-dose RYNX groups, with 10 rats in each group.A precancerous mammary lesion model was established for all groups except the control group.High-and low-dose RYNX cream containing TAM was coated on the breasts of animals in the corresponding groups.The rat mammary tissue was removed in the 10 th week and HIF-1α, HK2, PFK,PKM2 mRNA and protein was analyzed.RESULTS:In vitro analyses demonstrated that, compared with the matrix group, HIF-1α, HK2, PFK,PKM2 mRNA and protein expression was significantly decreased in the RYNX group(P < 0.05).Compared with the YC-1 + RYNX group, HK2, PFK,and PKM2 protein expression was significantly reduced in the RYNX group.HIF-1α, HK2, PFK, and PKM2 protein expression was increased significantly in the model group(P < 0.05) compared with the control group, while HIF-1α, HK2, PFK, and PKM2 mRNA and protein expression was significantly decreased in both the high-and low-dose RYNX groups(P < 0.05), with the effect being greater in the high-dose group.CONCLUSION:RYNX can block precancerous breast lesions by decreasing the expression of HK2,PFK, and PKM2 mRNA and protein via inhibition of HIF-1α mRNA and protein overexpression in a dose-dependent manner. | Li Xiaobo Ma Min Zhang Guijuan Ma Yi Liao Rui Chen Ruixue Yan Xianxin Bie Fengjie Huang Maojie Liang Shijie | 2017 | Journal of Traditional Chinese Medicine2017，37，2： | 5 |
| 4 | 基于网络药理学及分子对接探讨“柴胡-当归”药对治疗乳腺增生的作用机制显示文摘目的通过网络药理学和分子对接技术探索“柴胡-当归”药对治疗乳腺增生的潜在作用机制。方法基于网络药理学,通过TCMSP、UniProt等数据库检索获得“柴胡-当归”药对的活性成分及其对应靶点蛋白。在Genecards数据库检索乳腺增生相关靶点,利用Draw Venn Diagram在线作图网站获得其与“柴胡-当归”作用靶点的交集基因。通过Cytoscape 3.6.0软件及STRING数据库构建药对-活性成分-作用靶点-疾病网络和靶点间蛋白-蛋白相互作用(PPI)网络,根据度值大小筛选出排名前5的靶蛋白,并利用RCSB PDB数据库、Autodock Vina 1.1.2等软件预测其与“柴胡-当归”药对活性成分的结合活性。采用RStudio软件对交集基因进行GO富集分析和KEGG通路富集分析,最终构建活性成分-关键靶点-关键通路网络。结果数据库中筛选获得药对活性成分共18种;其中活性成分的靶点与乳腺增生疾病的交集基因共150个,根据度值排名大小获得5个核心靶标,包括蛋白激酶、白细胞介素-6、肿瘤蛋白p53、血管内皮生长因子A及肿瘤坏死因子等。经分子对接分析发现,“柴胡-当归”药对的活性成分与核心靶标结合能力较强。结论“柴胡-当归”药对的主要活性成分可能通过调节蛋白激酶、白细胞介素-6、肿瘤蛋白p53、血管内皮生长因子A及肿瘤坏死因子等核心靶点,参与调控白介素-7(IL-7)信号通路、内分泌耐药、丝裂原活化蛋白激酶(MAPK)信号通路、肿瘤坏死因子(TNF)信号通路、缺氧诱导因子1(HIF-1)信号通路等途径,发挥对乳腺增生的治疗作用。 | 袁名扬 周学刚 扈丹丹 蒋蕾 杨波 彭海生 | 2022 | 药学研究2022，41，2： | 4 |
| 5 | 负离子远红外功能织物对乳腺增生大鼠模型的影响显示文摘为探究负离子远红外功能织物对乳腺增生的保健效果,采用浸轧法制备负离子远红外功能织物,选取健康雌性SD大鼠为研究对象,随机分为对照组、模型组和功能织物组,功能织物组穿着由负离子远红外功能织物制成的外套,模型组穿着普通面料外套,采用公认的雌激素法制备乳腺增生大鼠模型。通过测量大鼠乳头高度和直径,进行乳腺组织形态学观察。结果表明:与对照组比较,模型组乳头直径、高度增大;与模型组比较,功能织物组乳头直径、高度减小;功能织物组较模型组乳腺形态和组织学特征有所改善;负离子远红外功能织物可使乳腺增生模型大鼠乳头高度、直径明显缩小,对大鼠乳腺增生有一定的抑制作用。 | 吴继辉 邹婉晴 汤明竹 沈小雨 杨佳敏 张露芬 | 2019 | 纺织学报2019，40，6： | 3 |
| 6 | 乳增消胶囊抗小鼠乳腺增生显示文摘目的研究乳增消胶囊抗小鼠乳腺增生作用。方法腹腔注射苯甲酸雌二醇建立小鼠乳腺增生疾病模型,以乳疾灵作为阳性对照组,受试药乳增消胶囊分为低、中、高(0.25、0.5、1.0 g/kg)剂量组,按组别灌胃30天,观察各组小鼠乳头直径、高度变化,测定小鼠血清雌二醇(E2)、孕酮(PROG)含量,并对乳腺组织进行病理组织学检查。结果乳增消胶囊显著降低乳腺增生小鼠的乳头高度和直径,病理组织学检查可见乳增消胶囊中、高剂量组乳腺小叶体积较模型组均有减小,腺管扩张程度下降。乳增消胶囊和乳疾灵均对乳腺增生小鼠血清雌二醇及孕酮含量未见明显影响。结论乳增消胶囊具有抑制乳腺增生的作用,且其作用强度与乳疾灵无明显差异。 | 何建 王健鑫 李果 朱久新 张妍 乔国芬 | 2016 | 哈尔滨医科大学学报2016，50，2： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员