Resveratrol-Mediated Reduction of Collagen by Inhibiting Proliferation and Producing Apoptosis in Human Hypertrophic Scar Fibroblasts

Zeng, Guofang; Fang, Zhong; Jin, Li; Luo, Sulan; Zhang, Peihua

doi:10.1271/bbb.130502

Cited by 29 publications

(34 citation statements)

References 44 publications

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“…In addition, the results of the present study suggested that the antiproliferative effect of resveratrol on eosinophils may be associated with cell cycle inhibition. Following exposure of eosinophils to 80 and 160 µM resveratrol, a greater percentage of cells in G 1 phase, and a reduced percentage of cells in S and G 2 /M phases were observed when compared with the untreated controls, which is similar to a previous report involving human hypertrophic scar fibroblasts (13). In order to investigate the mechanism of resveratrol-mediated cell cycle arrest in eosinophils further, the protein expression levels of p53, p21, CDK2, cyclin A and cyclin E were determined by western blotting.…”

Section: Discussionsupporting

confidence: 88%

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Resveratrol induces cell cycle arrest and apoptosis in human eosinophils from asthmatic individuals

Hu¹,

Wang²,

Xia³

et al. 2016

Molecular Medicine Reports

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Abstract. Eosinophils exert a number of inflammatory effects through the degranulation and release of intracellular mediators, and are considered to be key effector cells in allergic disorders, including asthma. In order to investigate the regulatory effects of the natural polyphenol, resveratrol, on eosinophils derived from asthmatic individuals, the cell counting Kit-8 assay and flow cytometry analysis were used to determine cell proliferation and cell cycle progression in these cells, respectively. Cellular apoptosis was detected using annexin V-fluorescein isothiocyanate/propidium iodide double-staining. The protein expression levels of p53, p21, cyclin-dependent kinase 2 (CDK2), cyclin A, cyclin E, Bim, B-cell lymphoma (Bcl)-2 and Bcl-2-associated X protein (Bax) were measured by western blot analysis following resveratrol treatment. The results indicated that resveratrol effectively suppressed the proliferation of eosinophils from asthmatic patients in a concentration-and time-dependent manner. In addition, resveratrol was observed to arrest cell cycle progression in G 1 /S phase by increasing the protein expression levels of p53 and p21, and concurrently reducing the protein expression levels of CDK2, cyclin A and cyclin E. Furthermore, resveratrol treatment significantly induced apoptosis in eosinophils, likely through the upregulation of Bim and Bax protein expression levels and the downregulation of Bcl-2 protein expression. These findings suggested that resveratrol may be a potential agent for the treatment of asthma by decreasing the number of eosinophils.

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Section: Discussionsupporting

confidence: 88%

“…Previously, it was reported that resveratrol notably inhibited the proliferation of fibroblasts from human hypertrophic scars, and decreased collagen expression in these cells (13). However, the effect of resveratrol on the proliferation and survival of human eosinophils isolated from asthmatic patients remains unclear.…”

Section: Introductionmentioning

confidence: 98%

Resveratrol induces cell cycle arrest and apoptosis in human eosinophils from asthmatic individuals

Hu¹,

Wang²,

Xia³

et al. 2016

Molecular Medicine Reports

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“…Curcumin was able to induce apoptosis in human dermal fibroblasts and inhibit fibroblast-mediated contraction, all via oxidative pathways [79]. In vitro findings demonstrate that resveratrol is capable of inhibiting fibroblast function, and it may prove effective in the treatment of hypertrophic scars or keloids in vivo [80, 81]. These compounds call for further research into the potential oxidative-associated clinical sequelae.…”

Section: Hypertrophic Scarsmentioning

confidence: 99%

Oxidative Stress and Skin Fibrosis

2014

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Fibrosis is defined as increased fibroblast proliferation and deposition of extracellular matrix components with potential clinical ramifications including organ dysfunction and failure. Fibrosis is a characteristic finding of various skin diseases which can have life-threatening consequences. These implications call for research into this topic as few treatments targeting fibrosis are available. In this review, we discuss oxidative stress and its role in skin fibrosis. Recent studies have implicated the importance of oxidative stress in a variety of cellular pathways directly and indirectly involved in the pathogenesis of skin fibrosis. The cellular pathways by which oxidative stress affects specific fibrotic skin disorders are also reviewed. Finally, we also describe various therapeutic approaches specifically targeting oxidative stress to prevent skin fibrosis. We believe oxidative stress is a relevant target, and understanding the role of oxidative stress in skin fibrosis will enhance knowledge of fibrotic skin diseases and potentially produce targeted therapeutic options.

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“…It can inhibit the proliferation of pathological scar fibroblasts via downregulating the expression of mammalian target of rapamycin (mTOR) /70S6K signaling pathway or TGF-β1, Smad-2, 3,4, and upregulating expression of Smad 7 [58,59]. It can also inhibited proliferation of hypertrophic scar-derived fibroblasts and adventitial fibroblast in vitro and led to a more organized and thinner collagen fibre in the mouse model of wound healing via up-regulating expression of Sirt1 [60][61][62]. Here, we showed that resveratrol could enhance viability of NIH3T3 cells via activating the Shh signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Activated Sonic Hedgehog Signaling to Enhance Viability of NIH3T3 Cells in Vitro via Regulation of Sirt1

Guo¹,

Liao²,

Liu³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Injuries of the brain and spinal cord result in the formation of glial (reactive gliosis) and fibrotic (formed by fibroblasts) scars. Recent studies have shown that the fibrotic scar was much more important for hindering regeneration after brain or spinal cord injury than the astrocytic scar. However, it has been given much less attention for effects and mechanism of fibroblasts during formation of the fibrotic scar. Resveratrol may be a potential anti-scarring agent in burn-related scarring and keloid fibroblasts. However, it is unclear whether and how resveratrol affects formation of the fibrotic scar after brain or spinal cord injury. Earlier studies have shown that the activated Shh signaling has anti-apoptosis, anti-oxidation, anti-inflammation properties. Moreover, resveratrol can activate the Shh signaling. However, it is unclear how resveratrol activates the Shh signaling. Resveratrol is a activator of Sirt1. It is unknown whether resveratrol activates the Shh signaling via Sirt1. Methods: NIH3T3 cells, a fibroblast cell line, were used as model cells and treated with drugs. Cell viability was assessed by Cell Counting Kit 8. The expressions and activity of Shh signaling pathway proteins were evaluated by immunocytochemistry and Western blotting. Transcriptional activity of Gli-1 was detected with Dual-Luciferase Reporter Gene Assay Kit. Results: Resveratrol, Sirt1 agonist STR1720 and recombinant mouse Shh protein, an activator of hedgehog signaling, enhanced the viability of NIH3T3 cells, promoted Smo to translocated to the primary cilia and Gli-1 entered into the nuclei from cytoplasm, and upregulated expressions of Shh, Ptc-1, Smo, and Gli-1 proteins, which can be reversed by Smo antagonist cyclopamine and Sirt1 antagonist Sirtinol. Additionally, resveratrol increased transcriptional activity of Gli-1. Conclusion: We indicate in the first time that it may be mediated by Sirt1 for resveratrol activating the Shh signaling to enhance viability of NIH3T3 cells, and Sirt1 may be a regulator for upstream of the Shh signaling pathway.This study provides a basis for further investigating effects and mechanism of resveratrol during the formation of fibrous scar after brain or spinal cord injury.

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Resveratrol-Mediated Reduction of Collagen by Inhibiting Proliferation and Producing Apoptosis in Human Hypertrophic Scar Fibroblasts

Cited by 29 publications

References 44 publications

Resveratrol induces cell cycle arrest and apoptosis in human eosinophils from asthmatic individuals

Resveratrol induces cell cycle arrest and apoptosis in human eosinophils from asthmatic individuals

Oxidative Stress and Skin Fibrosis

Resveratrol Activated Sonic Hedgehog Signaling to Enhance Viability of NIH3T3 Cells in Vitro via Regulation of Sirt1

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