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地奥司明与橙皮苷微粉化纯化黄酮类成分(MPFF)在治疗慢性静脉疾病中的治疗潜力

[Therapeutic potential of micronized purified flavonoid fraction (MPFF) of diosmin and hesperidin in treatment chronic venous disorder].

作者信息

Hnátek Lukáš

出版信息

Vnitr Lek. 2015 Sep;61(9):807-14.

PMID:26465280
Abstract

Chronic venous disorder (CVD) is a common illness with high incidence existing especially in Europe and North America. The main goal of micronized purified flavonoid fraction (MPFF) of diosmin and hesperidin is to eliminate the symptoms of CVD (venous pain, fatigue, etc). But MPFF of diosmin and hesperidin has good effectiveness for treatment of venous oedema and venous ulcer too. There are many papers that prove its effectiveness in the experiment and in the microcirculation too. The other indications for MPFF of diosmin hesperidin is hemorrhoidal disease and the accessory treatment of lymphedema. It is proved that this substance could be used as an effective supplementary treatment of symptoms after venous intervention. Only MPFF diosmin and hesperidin received the best recommendation - 1B in the last guidelines for VAD therapy.

摘要

慢性静脉疾病(CVD)是一种常见疾病,发病率很高,尤其在欧洲和北美地区。地奥司明和橙皮苷微粉化纯化黄酮组分(MPFF)的主要目标是消除CVD的症状(静脉疼痛、疲劳等)。但地奥司明和橙皮苷的MPFF对治疗静脉水肿和静脉溃疡也有良好疗效。有许多论文证明了其在实验和微循环中的有效性。地奥司明橙皮苷MPFF的其他适应症是痔疮疾病和淋巴水肿的辅助治疗。事实证明,这种物质可作为静脉介入术后症状的有效辅助治疗。在最新的VAD治疗指南中,只有地奥司明和橙皮苷MPFF获得了最佳推荐——1B级。

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[Therapeutic potential of micronized purified flavonoid fraction (MPFF) of diosmin and hesperidin in treatment chronic venous disorder].地奥司明与橙皮苷微粉化纯化黄酮类成分(MPFF)在治疗慢性静脉疾病中的治疗潜力
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引用本文的文献

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Diosmin Promotes Myogenesis via Activating the Akt/FOXO1 Pathway to Facilitate the Proliferation of C2C12 Myoblasts.地奥司明通过激活 Akt/FOXO1 通路促进成肌分化,从而促进 C2C12 成肌细胞的增殖。
J Agric Food Chem. 2023 Dec 13;71(49):19705-19716. doi: 10.1021/acs.jafc.3c04828. Epub 2023 Nov 29.
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The synergistic anti-proliferative effect of the combination of diosmin and BEZ-235 (dactolisib) on the HCT-116 colorectal cancer cell line occurs through inhibition of the PI3K/Akt/mTOR/NF-κB axis.地奥司明与 BEZ-235(达妥昔单抗)联合对 HCT-116 结直肠癌细胞系的协同抗增殖作用是通过抑制 PI3K/Akt/mTOR/NF-κB 轴实现的。
Mol Biol Rep. 2020 Mar;47(3):2217-2230. doi: 10.1007/s11033-020-05327-4. Epub 2020 Feb 22.