首页> 美国卫生研究院文献>Evidence-based Complementary and Alternative Medicine : eCAM >Potential Mechanisms of an Antiadenomyosis Chinese Herbal Formula Shaoyao-Gancao Decoction in Primary Cell Culture Model
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Potential Mechanisms of an Antiadenomyosis Chinese Herbal Formula Shaoyao-Gancao Decoction in Primary Cell Culture Model

机译:抗子宫腺肌病中药Sha药-甘草汤在原代细胞培养模型中的潜在机制

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摘要

Background. Shaoyao-Gancao Decoction (SGD), a well-known traditional Chinese medicine prescription, has been widely used to treat adenomyosis, dysmenorrhea, abdominal pain, and inflammation in Asia. However, the mechanism underlying the effectiveness of SGD in the treatment of adenomyosis still remains elusive. The present study aimed to investigate the bioactivity of SGD and its underlying molecular mechanisms using cultured human adenomyosis-derived cells. Methods. Human adenomyosis-derived cells were treated with SGD and its major constituents (paeoniflorin and liquiritin) in vitro. Effects of SGD, paeoniflorin, and liquiritin on cell proliferation and apoptosis were examined by MTT assay and flow cytometry analyses. The effects of SGD, paeoniflorin, and liquiritin on the production of PGE2 and PGF2α were assayed using ELISA. ER-α and OTR mRNA expression levels were also evaluated by real-time qRT-PCR. Results. SGD, paeoniflorin, and liquiritin inhibited proliferation and induced apoptosis of human adenomyosis-derived cells in a dose-dependent manner. SGD and paeoniflorin significantly reduced the PGE2 and PGF2α production. Furthermore, they remarkably decreased the mRNA levels of ER-α and OTR. Conclusions. The results of this study provide possible mechanisms for the bioactivity of SGD for treating adenomyosis and contribute to the ethnopharmacological knowledge about this prescription.
机译:背景。邵药甘草汤(SGD)是一种著名的中药处方,在亚洲已被广泛用于治疗子宫腺肌病,痛经,腹痛和炎症。但是,SGD治疗子宫腺肌病的有效性的机制仍不清楚。本研究旨在调查培养的人子宫腺肌病来源的细胞SGD的生物活性及其潜在的分子机制。方法。在体外用SGD及其主要成分(pa药苷和脂蛋白)处理人子宫腺肌病来源的细胞。通过MTT分析和流式细胞术分析检查了SGD,pa药苷和脂蛋白对细胞增殖和凋亡的影响。用ELISA测定了SGD,pa药苷和脂蛋白对PGE2和PGF2α产生的影响。还通过实时qRT-PCR评估了ER-α和OTR mRNA表达水平。结果。 SGD,pa药苷和liquiritin以剂量依赖的方式抑制人子宫腺肌病衍生细胞的增殖并诱导其凋亡。 SGD和pa药苷显着降低了PGE2和PGF2α的产生。此外,它们显着降低了ER-α和OTR的mRNA水平。结论。这项研究的结果为SGD治疗子宫腺肌病的生物活性提供了可能的机制,并为有关该处方的民族药理学知识做出了贡献。

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