Resveratrol accelerates wound healing by attenuating oxidative stress-induced impairment of cell proliferation and migration

Burns ◽  
2020 ◽  
Author(s):  
Xueqing Zhou ◽  
Qiongfang Ruan ◽  
Ziqing Ye ◽  
Zhigang Chu ◽  
Maomao Xi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Wound Healing ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals LncRNA XIST promotes extracellular matrix synthesis, proliferation and migration by targeting miR-29b-3p/COL1A1 in human skin fibroblasts after thermal injury

2019 ◽  
Vol 52 (1) ◽  
Author(s):  
Wei Cao ◽  
Youping Feng
Keyword(s):  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Wound Healing ◽  
Western Blot ◽  
Thermal Injury ◽  
Human Skin Fibroblasts ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Long noncoding RNAs (lncRNAs) have been reported to be associated with dermis process during burn wound healing. This study aimed to investigate the role of lncRNA X-inactive specific transcript (XIST) in human skin fibroblasts (HSF) and extracellular matrix (ECM) as well as the regulatory network of XIST/microRNA-29b-3p (miR-29b-3p)/collagen 1 alpha 1 (COL1A1). Methods The wound samples were collected from 25 patients with deep partial thickness burn at day 5 after burn. The thermal injured model was established using HSF cells. The expressions of XIST, miR-29b-3p and COL1A1 were measured by quantitative real-time polymerase chain reaction and western blot. ECM synthesis, cell proliferation and migration were detected by western blot, cell counting kit-8 and trans-well assays, respectively. The interaction between miR-29b-3p and XIST or COL1A1 was explored by bioinformatics analysis and luciferase reporter assay. Results The expressions of XIST and COL1A1 were enhanced but miR-29b-3p expression was decreased after thermal injury. XIST overexpression promoted ECM synthesis, cell proliferation and migration in thermal injured HSF cells. However, XIST knockdown played an opposite effect. miR-29b-3p overexpression inhibited ECM synthesis, cell proliferation and migration, which was reversed by XIST. COL1A1 silence suppressed ECM synthesis, cell proliferation and migration by miR-29b-3p targeting. Moreover, COL1A1 up-regulation weakened the effect of XIST silence on ECM synthesis and HSF cell function. Conclusion XIST promoted ECM synthesis, cell proliferation and migration by sponging miR-29b-3p and targeting COL1A1 in HSF cells after thermal injury, indicating the promoting role of XIST in wound healing.

scholarly journals Inhibition of myeloperoxidase increases revascularization and improves blood flow in a diabetic mouse model of hindlimb ischaemia

2020 ◽  
Vol 17 (3) ◽  
pp. 147916412090797 ◽  
Author(s):  
Dorothee Weihrauch ◽  
Dustin P Martin ◽  
Deron Jones ◽  
John Krolikowski ◽  
Janine Struve ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Blood Flow ◽  
Endothelial Cell ◽  
Neutrophil Infiltration ◽  
Endothelial Cell Proliferation ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Objective: Diabetes mellitus is a significant risk factor for peripheral artery disease. Diabetes mellitus induces chronic states of oxidative stress and vascular inflammation that increase neutrophil activation and release of myeloperoxidase. The goal of this study is to determine whether inhibiting myeloperoxidase reduces oxidative stress and neutrophil infiltration, increases vascularization, and improves blood flow in a diabetic murine model of hindlimb ischaemia. Methods: Leptin receptor–deficient ( db/db) mice were subjected to hindlimb ischaemia. Ischaemic mice were treated with N-acetyl-lysyltyrosylcysteine-amide (KYC) to inhibit myeloperoxidase. After ligating the femoral artery, effects of treatments were determined with respect to hindlimb blood flow, neutrophil infiltration, oxidative damage, and the capability of hindlimb extracellular matrix to support human endothelial cell proliferation and migration. Results: KYC treatment improved hindlimb blood flow at 7 and 14 days in db/db mice; decreased the formation of advanced glycation end products, 4-hydroxynonenal, and 3-chlorotyrosine; reduced neutrophil infiltration into the hindlimbs; and improved the ability of hindlimb extracellular matrix from db/db mice to support endothelial cell proliferation and migration. Conclusion: These results demonstrate that inhibiting myeloperoxidase reduces oxidative stress in ischaemic hindlimbs of db/db mice, which improves blood flow and reduces neutrophil infiltration such that hindlimb extracellular matrix from db/db mice supports endothelial cell proliferation and migration.

scholarly journals Wound healing promoting activity of Earthworm, Eutyphoeus gammiei (Beddard): in vitro studies on human skin keratinocyte cell line (HaCat).

2018 ◽  
Vol 8 (6) ◽  
pp. 155-158
Author(s):  
Susmita Saha ◽  
Deepjyoti Bhattacharjee ◽  
Anwesha Saha ◽  
Gahin De ◽  
Partha Saha ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Cell Line ◽  
Key Factors ◽  
Cell Proliferation And Migration ◽  
Keratinocyte Cell Line Hacat ◽  
Keratinocyte Cell ◽  
And Migration ◽  
Proliferation And Migration

Earthworm, Eutyphoeus gammiei, homogenate (EGH) was screened for wound healing activity on human keratinocyte cell line, HaCat, by cell proliferation and migration assays. The maximum proliferation and migration of keratinocyte cells were observed at the dose of 25μg/ml. As cell proliferation and migration are key factors for wound healing, the study clearly suggests the potential role of earthworm species Eutyphoeus gammiei on wound healing. Keywords: Eutyphoeus gammiei, Keratinocyte, MTT assay, scratch assay.

scholarly journals Tea polyphenol EGCG inhibited colorectal-cancer-cell proliferation and migration via downregulation of STAT3

2020 ◽  
Author(s):  
Ke-Wang Luo ◽  
Jun Xia ◽  
Bao-Hui Cheng ◽  
Han-Chao Gao ◽  
Li-Wu Fu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Cell Proliferation ◽  
Wound Healing ◽  
Promoter Activity ◽  
Luciferase Reporter ◽  
Cell Proliferation And Migration ◽  
Migration Assays ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Green tea is a popular beverage worldwide and epigallocatechin-3-gallate (EGCG) is the most bioactive polyphenol in green tea. Our study aims to investigate the anti-proliferation and anti-migration effects of EGCG against colorectal-cancer SW480, SW620, and LS411N cells, and elucidate the underlying mechanism. Methods The in vitro anti-proliferation and anti-migration effects of EGCG against colon-cancer cells were evaluated using MTT, scratch-wound-healing, and transwell-migration assays. The effects of EGCG on apoptosis were assessed by Annexin V-FITC/PI double staining and JC-1 staining. Besides, Western blotting was employed to detect the protein-expression level and elucidate the underlying pathways. Real-time qPCR and dual-luciferase reporter assay were adopted to determine the mRNA level and promoter activity. Results Our results demonstrated that treatment with EGCG resulted in significant inhibition of cell proliferation by the induction of apoptosis. EGCG also inhibited SW480 cell migration in a dose-dependent manner as assessed by wound-healing and transwell-migration assays. Western blot confirmed that EGCG induced apoptosis by the activation of Caspase-3 and PARP. In addition, both STAT3 and phosphorylated STAT3 (p-STAT3) were downregulated significantly by EGCG in three selected colorectal-cancer cell lines. EGCG treatment also resulted in a significant decrease in Bcl-2, MCL-1, and Vimentin, and an increase in E-cadherin. When STAT3 was inhibited, EGCG showed no obvious effect on cell proliferation and migration. Further investigation by luciferase-reporter-activity assay showed that EGCG suppressed the promoter activity of STAT3 and downregulated the transcription of STAT3. Conclusion Our study presents evidence on the anti-proliferation and anti-migration effects of EGCG against colorectal-cancer SW480, SW620, and LS411N cells by downregulating the expression of STAT3 and suggests that EGCG could be an effective and natural supplement for colon-cancer treatment.

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