Combination of ginsenoside Rb1 and Rd protects the retina against bright light-induced degeneration.

Combination of ginsenoside Rb1 and Rd protects the retina against bright light-induced degeneration.
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人参皂苷 Rb1 和 Rd 的组合可保护视网膜免受强光引起的变性

DOI:
10.1038/s41598-017-06471-x
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发表时间:
2017-07-20
期刊:
影响因子:
4.6
通讯作者:
Chen Y
Chen Y
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Bian M;Du X;Wang P;Cui J;Xu J;Gu J;Zhang T;Chen Y

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光感受器变性是目前缺乏有效治疗的各种视网膜变性疾病的中心病理。三七皂苷(PNS)和相关皂苷化合物具有抗氧化和抗炎活性。然而,PNS或相关皂苷化合物的光感受器保护潜力仍然未知。目前的研究表明,三七总皂苷对强光暴露的BALB/c小鼠的感光细胞损失的保护。PNS中两种主要的皂苷类化合物Rb 1和Rd的联合应用,重现了PNS的视网膜保护作用,减轻了视网膜氧化应激和炎症反应。Rb 1或Rd部分减轻全反式-Retinal诱导的ARPE 19细胞氧化应激。Rb 1或Rd抑制脂多糖(LPS)诱导的ARPE 19和RAW 264.7细胞中的促炎基因表达。Rb 1或Rd还调节脂多糖刺激的RAW264.7细胞中促炎微小RNA(miR-155)及其直接靶点(抗炎SHIP 1)的表达。视网膜损伤前miR-155和SHIP 1的表达发生改变,Rb 1和Rd联合用药后维持在正常水平。这项工作首次表明miR-155和SHIP 1的表达改变参与了感光细胞变性。最重要的是,Rb 1和Rd组合的新型视网膜保护活性证明了进一步评价相关视网膜退行性疾病的治疗是合理的。
Photoreceptor degeneration is a central pathology of various retinal degenerative diseases which currently lack effective therapies. Antioxidant and anti-inflammatory activities are noted for Panax notoginsenoside saponins (PNS) and related saponin compound(s). However, the photoreceptor protective potentials of PNS or related saponin compound(s) remain unknown. The current study revealed that PNS protected against photoreceptor loss in bright light-exposed BALB/c mice. Combination of ginsenoside Rb1 and Rd, two major saponin compounds of PNS, recapitulated the retinal protection of PNS and attenuated retinal oxidative stress and inflammatory changes. Rb1 or Rd partially alleviated all-trans-Retinal-induced oxidative stress in ARPE19 cells. Rb1 or Rd suppressed lipopolysaccharides (LPS)-induced proinflammatory gene expression in ARPE19 and RAW264.7 cells. Rb1 or Rd also modulated the expression of proinflammatory microRNA, miR-155 and its direct target, anti-inflammatory SHIP1, in LPS-stimulated RAW264.7 cells. The retinal expression of miR-155 and SHIP1 was altered preceding extensive retinal damage, which was maintained at normal level by Rb1 and Rd combination. This work shows for the first time that altered expression of miR-155 and SHIP1 are involved in photoreceptor degeneration. Most importantly, novel retinal protective activities of combination of Rb1 and Rd justify further evaluation for the treatment of related retinal degenerative disorders.
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