Abstract：
UNASSIGNED: To evaluate the effects of various initiation time points and durations of hormone therapy (HT) on cardiovascular and metabolic parameters of premenarche, primary ovarian insufficiency (POI) mouse model, induced by 4-vinylcyclohexene diepoxide.
UNASSIGNED: A total of 50 mice at 4 weeks of age were developed into POI mouse model, further randomly categorized into 5 groups: control group without any intervention; no HT group with only high-fat diet (NT); group 1 with delayed estradiol treatment (T1); group 2 with on-time, continuous estradiol treatment (T2); and group 3 with on-time estradiol treatment but early stop (T3). Cardiovascular risk and metabolic parameters were measured.
UNASSIGNED: Presenting with similar body weights, blood glucose levels of T1, T2, and T3 were all significantly lower than NT (p < .001). Serum total cholesterol and insulin were also significantly lower in all HT groups than in NT, especially in T2 (p < .001). For serum low-density lipoprotein-cholesterol, only T2 resulted in the statically lower level than those of NT, T1, and T3 (p < .001). Aortic thickness was significantly increased with aggravated fibrotic change of the intima in NT, and such consequence was significantly ameliorated in HT groups, mostly lowered in T2 (p < .05). Last, serum pro-inflammatory cytokines were significantly low in the HT groups than in NT, especially in T2 with the lowest level (p < .05). .
UNASSIGNED: On-time, continuous E2 treatment immediately after a biologic estrogen deprivation event significantly reduced metabolic and cardiovascular risks in young, pre-menarche female mouse models of POI, confirming decreased serum levels of pro-inflammatory cytokines.
UNASSIGNED: A total of 50 mice at 4 weeks of age were developed into POI mouse model, further randomly categorized into 5 groups: control group without any intervention; no HT group with only high-fat diet (NT); group 1 with delayed estradiol treatment (T1); group 2 with on-time, continuous estradiol treatment (T2); and group 3 with on-time estradiol treatment but early stop (T3). Cardiovascular risk and metabolic parameters were measured.
UNASSIGNED: Presenting with similar body weights, blood glucose levels of T1, T2, and T3 were all significantly lower than NT (p < .001). Serum total cholesterol and insulin were also significantly lower in all HT groups than in NT, especially in T2 (p < .001). For serum low-density lipoprotein-cholesterol, only T2 resulted in the statically lower level than those of NT, T1, and T3 (p < .001). Aortic thickness was significantly increased with aggravated fibrotic change of the intima in NT, and such consequence was significantly ameliorated in HT groups, mostly lowered in T2 (p < .05). Last, serum pro-inflammatory cytokines were significantly low in the HT groups than in NT, especially in T2 with the lowest level (p < .05). .
UNASSIGNED: On-time, continuous E2 treatment immediately after a biologic estrogen deprivation event significantly reduced metabolic and cardiovascular risks in young, pre-menarche female mouse models of POI, confirming decreased serum levels of pro-inflammatory cytokines.
摘要：
■为了评估激素治疗（HT）的各种起始时间点和持续时间对初潮的心血管和代谢参数的影响，原发性卵巢功能不全(POI)小鼠模型,由4-乙烯基环己烯二环氧化物诱导。
■将总共50只4周龄的小鼠发展成POI小鼠模型，进一步随机分为5组：对照组，无任何干预;无HT组，仅高脂饮食（NT）;第1组，延迟雌二醇治疗（T1）;第2组，持续雌二醇治疗（T2）；第3组按时进行雌二醇治疗，但提早停止（T3）。测量心血管风险和代谢参数。
■呈现相似的体重，T1、T2和T3的血糖水平均显著低于NT(p<.001)。血清总胆固醇和胰岛素在所有HT组也显著低于NT，特别是在T2（p<.001）。对于血清低密度脂蛋白胆固醇，只有T2导致静态低于NT的水平，T1和T3(p<.001)。随着NT内膜纤维化改变的加重，主动脉厚度明显增加，这种后果在HT组中得到了显着改善，大部分在T2降低（p<0.05）。最后,血清促炎细胞因子在HT组显著低于NT组,特别是在T2的最低水平（p<0.05）。.
■准时，在发生生物雌激素剥夺事件后立即连续E2治疗可显著降低年轻人的代谢和心血管风险,月经初潮前POI的雌性小鼠模型，证实血清促炎细胞因子水平降低。
■将总共50只4周龄的小鼠发展成POI小鼠模型，进一步随机分为5组：对照组，无任何干预;无HT组，仅高脂饮食（NT）;第1组，延迟雌二醇治疗（T1）;第2组，持续雌二醇治疗（T2）；第3组按时进行雌二醇治疗，但提早停止（T3）。测量心血管风险和代谢参数。
■呈现相似的体重，T1、T2和T3的血糖水平均显著低于NT(p<.001)。血清总胆固醇和胰岛素在所有HT组也显著低于NT，特别是在T2（p<.001）。对于血清低密度脂蛋白胆固醇，只有T2导致静态低于NT的水平，T1和T3(p<.001)。随着NT内膜纤维化改变的加重，主动脉厚度明显增加，这种后果在HT组中得到了显着改善，大部分在T2降低（p<0.05）。最后,血清促炎细胞因子在HT组显著低于NT组,特别是在T2的最低水平（p<0.05）。.
■准时，在发生生物雌激素剥夺事件后立即连续E2治疗可显著降低年轻人的代谢和心血管风险,月经初潮前POI的雌性小鼠模型，证实血清促炎细胞因子水平降低。
