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作 者:林妮[1] 吕俊华[2] 潘竞锵[3,4] 肖柳英[3,4]
机构地区:[1]广州市中医医院药剂科,广州市510130 [2]暨南大学药学院药理研究室,广州市510632 [3]广州市中医医院 [4]广州市中医中药研究所药理研究室,广州市510130
出 处:《中国药房》2010年第11期975-977,共3页China Pharmacy
基 金:广州市中医药中西医结合科研课题(2006A15)
摘 要:目的:研究荔枝核提取物抑制乳腺增生(HMG)模型大鼠乳腺组织雌二醇受体(ER)和孕酮受体(PR)表达及促进乳腺细胞凋亡的作用。方法:肌肉注射苯甲酸雌二醇0.5mg·kg-1连续25d后,改肌肉注射黄体酮4mg·kg-1连续5d,复制大鼠HMG模型。取健康、未孕雌性SD大鼠60只,均分为6组,即正常(蒸馏水)、模型(蒸馏水)、乳结平(3.3g·kg-1)及荔枝核提取物高、中、低剂量(44、22、11g·kg-1)组,ig给药,每天1次,连续给药30d。通过免疫组化方法观察大鼠乳腺组织中ER和PR的表达情况,流式细胞仪检测乳腺组织细胞凋亡情况,并计算子宫指数。结果:高、中剂量荔枝核提取物能显著抑制HMG模型大鼠乳腺中ER和PR表达(P<0.01或P<0.05),显著促进乳腺细胞凋亡(P<0.01或P<0.05)。HMG大鼠乳头红肿及增生明显,子宫指数显著增加(P<0.01),而各给药组能不同程度地逆转上述病理性改变(P<0.05或0.01)。结论:荔枝核提取物能抑制HMG模型大鼠乳腺组织ER和PR表达,并促进乳腺细胞凋亡,改善HMG及子宫的病理变化,从而有效地对抗雌激素性大鼠HMG。OBJECTIVE: To study the effects of extracts of the seed of Litchi (ESL) on the expression of estradiol receptor (ER) and progestogen receptor (PR) in mammary tissue and apoptosis of mammary glandular cells in rats with hyperplasia of mammary glands (HMG). METHODS: The HMG model was induced by intramuscularly injecting with 0.5 mg. kg^-1 estradiol benzoate for 25 days, subsequently intramuscularly injecting with 4 mg.kg^-1 progesterone for 5 days. 60 healthy nonfertile SD rats were divided into normal group, model group, rujieping group and high-dose, medium-dose and low-dose ESL groups, treating with distilled water, distilled water, 3.3 g . kg ^-1 Rujieping and 44, 22, 11 g . kg^-1 ESL via i.g. gtt once a day for 30 days, respectively. Immunohistochemical method was applied to observe the expression of ER and PR in rat mammary tissue and apoptosis of mammary glandular cells. Uterus index was also calculated. RESULTS: High-dose and medium-dose of ESL can inhibit the expression of ER and PR of mammary gland in HMG rats and induce apoptosis of mammary glandular cells(P〈0.01 or P〈0.05). Redness, swelling and hyperplasia of nipple in rats occurred and uterus index increased significantly (P〈0.01). Above pathological symptom was deteriorated to some extent in each group (P〈0.01 or P〈0.05). CONCLUSION: ESL can inhibit the expression of ER and PR, induce the apoptosis of mammary glandular cells and relieve the pathological symptom of uterus and HMG so as to inhibit estrogen HMG in rats.
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