The healing and anti-scar effects of astragaloside IV on the wound repair in vitro and in vivo

Chen, Xi; Peng, Li‐Hua; Li, Ni; Li, Qimei; Li, Ping; Fung, Kwok‐Pui; Leung, Ping‐Chung; J, Gao

doi:10.1016/j.jep.2011.11.035

Cited by 91 publications

(60 citation statements)

References 24 publications

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“…3G and 3H). These results indicated that the inhibitory effect of AS-IV on TGF-β1-induced HMrSV5 cell EMT is mediated by the suppression of Smad2/3 activation, which is consistent with previously published data on other epithelial cells [12,30].…”

Section: Discussionsupporting

confidence: 93%

“…1) is a saponin purified from Astragalus membranaceus that has been routinely used to treat various diseases in China [11]. It has been reported that AS-IV has healing and anti-scar effects on wound repair, and the accepted underlying mechanisms include both promoting angiogenesis and collagen synthesis and decreasing the levels of collagen I/III and TGF-β1 secretion by fibroblasts [12]. Moreover, AS-IV shows anti-fibrotic effects on renal fibrosis, hepatic fibrogenesis and myocardial fibrosis [13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

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Effects of Astragaloside IV Against the TGF-β1-Induced Epithelial-to-Mesenchymal Transition in Peritoneal Mesothelial Cells by Promoting Smad 7 Expression

Zhang

et al. 2015

Cell Physiol Biochem

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Background/Aims: To investigate the effect of Astragaloside IV (AS-IV) on the regulation of the TGF-β1/Smad signaling pathway in peritoneal mesothelial cells with an epithelial-to-mesenchymal transition (EMT). Methods: EMT of human peritoneal mesothelial cells (HMrSV5) was induced using 2 ng/ml TGF-β1. Cells were randomly divided into a vehicle group, a vehicle group with AS-IV, a TGF-β1 treated group, and a TGF-β1 treated group receiving varied doses of AS-IV or NAC. Real-time quantitative PCR and western blot were used to detect the expression of genes and proteins associated with the TGF-β1/Smad signaling pathway and EMT. DCFH-DA was used to detect the generation of ROS in HMrSV5 cells, and a transwell migration assay was used to verify the capacity of AS-IV to inhibit EMT in HMrSV5 cells. Lentiviruses were used as carriers for the overexpression or knockdown of the Smad7 gene. Results: Expression levels of E-cadherin (epithelial marker) was decreased and vimentin, α-SMA (EMT markers) and collagen I (extracellular matrix protein) phospho-Smad2/3, Snail1 and Snail2 was increased significantly in the TGF-β1-treated HMrSV5 cells. AS-IV was associated with downregulated expression of vimentin and phospho-Smad2/3 in a dose-dependent manner, while the expression of Smad7 increased. Silenced or forced expression of Smad7 verified its role in the inhibitory effect of AS-IV on TGF-β1-induced EMT in HMrSV5 cells. Conclusion: AS-IV effectively promotes the upregulation of Smad7 in the TGF-β1/Smad signaling pathway during the EMT of HMrSV5 cells, indicating its potential therapeutic effect for the control of PF.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Effects of Astragaloside IV Against the TGF-β1-Induced Epithelial-to-Mesenchymal Transition in Peritoneal Mesothelial Cells by Promoting Smad 7 Expression

Zhang

et al. 2015

Cell Physiol Biochem

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“…Furthermore, in our preliminary study, compared with the blank control, it was found that the topical application of astragaloside IV solution on rat wounds can significantly promote the regeneration of blood vessels in wound site. 19) In present study, in contrast to the wide areas of dense dermis devoid of skin appendage with the characteristics of scar in blank control and gel control, the appendages (indicated in the white arrows) in the healed skins with the structures of blood vessels were identified in both the astragaloside IV solution and hydrogel treated groups.…”

Section: Discussioncontrasting

confidence: 58%

“…Recently, we have demonstrated the significant stimulation of the astragalosides IV on wound repair and regeneration, which reminded the great potential of this compound on clinical wound treatment. 19) In present study, astragalosides IV-sustained releasing hydrogel was designed to decrease the degradability of astragalosides IV to the elements of heat, acid, etc. in the wound pathological environment upon topical application.…”

mentioning

confidence: 99%

Topical Astragaloside IV-Releasing Hydrogel Improves Healing of Skin Wounds <i>in Vivo</i>

Peng

Chen

et al. 2012

Biological & Pharmaceutical Bulletin

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Topical delivery of therapeutic agents at the time of injury to accelerate skin repair and prevent the formation of scars during the wound healing process has received increasing attention and represents a novel regenerative and prophylactic strategy for wound treatment. The aim of this study was to invesigate, for the first time, the influence of topical astragaloside IV-releasing hydrogel on the wound repair and regeneration. Using the sodium alginate-gelatin as a hydrogel vehicle, the astragaloside IV was incorporated into the topical carrier and kept releasing with a sustained manner at the wound site. With the rat skin excision model, regulation of the astragaloside IV hydrogel on the wound repair and regeneration were investigated. It was found that the astragaloside IV hydrogel was effective in the skin wound repair, leading to a significant improvement on the wound closure, collagen synthesis and skin tensile strength recovery. Meanwhile, for the first time, that functions of astragaloside IV hydrogel in activating the skin appendages regeneration and increasing the transforming growth factor-β 1 (TGF-β 1 ) level in serum were shown. Results of this study provided evidence for the alginate-gelatin hydrogel as efficient carrier for the topical delivery of bioactive molecules to the injured site. The astragaloside IV releasing hydrogel was shown a promising therapeutic formulation for wound healing, as well as its regenerative feature and underlying mechanism contribute to the skin regeneration were disclaimed.

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“…Astragaloside IV consistently suppressed collagen production in activated hepatic stellate cells via the oxidative stress-mediated p38 MAPK pathway [15]. Further, Astragaloside IV attenuates myocardial fibrosis by inhibiting TGF-β signaling [11] and exerts healing and anti-scar effects useful in wound treatment [16,17]. However, information about the efficacy of Astragaloside IV in the treatment of systemic sclerosis (SSc) is limited.…”

Section: Introductionmentioning

confidence: 99%

Anti-Fibrotic Effects of Astragaloside IV in Systemic Sclerosis

Mao

et al. 2014

Cell Physiol Biochem

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Objective: To evaluate the anti-fibrotic effects of Astragaloside IV in systemic sclerosis. Methods: Treated or untreated systemic sclerosis (SSc) and normal fibroblast isolated from corresponding pairs were utilized to detect expression of collagen and fibronectin by western blot, quantitative real-time RT-PCR (RT-qPCR), immunofluorescence staining and histopathological examination. SSc mouse model induced by bleomycin was used to evaluate the effects of the drug in vivo. Results: Compared to normal fibroblast (NF), the expression of collagen and fibronectin in SSc (SScF) dramatically increased, and this could be reduced by Astragaloside IV (AST) in a dose- or time-dependent manner at both protein and mRNA levels. Administration of Astragaloside IV consistently decreased collagen formation and partially restored the structure, as well as suppressing collagen and fibronectin expression in the skin lesions of SSc-model mice. Mechanistically, Astragaloside IV-induced fibrosis reduction may be due to deregulation of Smad 3/Fli-1, the major mediators of the fibrotic response and key molecules for TGF-β signaling. Astragaloside IV also decreased the level of p-SMAD3 and completely blocked its relocation into the nuclei. Conclusion: Astragaloside IV attenuates fibrosis by inhibiting the TGF-β-Smads3 axis in systemic sclerosis.

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The healing and anti-scar effects of astragaloside IV on the wound repair in vitro and in vivo

Cited by 91 publications

References 24 publications

Effects of Astragaloside IV Against the TGF-β1-Induced Epithelial-to-Mesenchymal Transition in Peritoneal Mesothelial Cells by Promoting Smad 7 Expression

Effects of Astragaloside IV Against the TGF-β1-Induced Epithelial-to-Mesenchymal Transition in Peritoneal Mesothelial Cells by Promoting Smad 7 Expression

Topical Astragaloside IV-Releasing Hydrogel Improves Healing of Skin Wounds <i>in Vivo</i>

Anti-Fibrotic Effects of Astragaloside IV in Systemic Sclerosis

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