Caffeic acid phenethyl ester promotes wound healing of mice pressure ulcers affecting NF-κB, NOS2 and NRF2 expression

Romana‐Souza, Bruna; Santos, Jeanine Salles dos; Monte‐Alto‐Costa, Andréa

doi:10.1016/j.lfs.2018.05.057

Cited by 43 publications

(28 citation statements)

References 59 publications

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“…Next, we observed that emodin decreased apoptosis (p < .05, Figure 2(C)) and inhibited these apoptotic proteins cleaved-poly (ADP-ribose) polymerase (PARP), cleaved-caspae-3 and cleaved-caspase-3 expression (p < .05, Figure 2(D,E)). In addition, the inflammation related factors IL-1b and IL-6 ( Figure 2 NF-jB signal pathway was blocked and PTEN/PI3K/AKT signal was inactivated by emodin NF-jB and PTEN/PI3K/AKT signal pathways were involved in pressure ulcers [25,26]. Our data revealed that LPS strengthened the phosphorylation of p65 and IjBa (p < .05, Figure 3(A,B)).…”

Section: Lps-induced Inflammation Was Alleviated By Emodinmentioning

confidence: 61%

Emodin protects against lipopolysaccharide-induced inflammatory injury in HaCaT cells through upregulation of miR-21

Song

Cui

Zhao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Background/aim: Pressure ulcers are a disastrous health issue in which inflammation is involved. Emodin possesses biological properties in inflammation. Our study investigated functions of emodin in lipopolysaccharide (LPS)-treated HaCaT cells. Methods: LPS was used to induce cell inflammation. MTT and flow cytometry were applied for cell viability and apoptosis assays, respectively. Moreover, apoptotic proteins were detected by western blot. Similarly, inflammatory factors and signalling related proteins were also determined by western blot. Results: Emodin increased cell viability and diminished apoptosis in LPS-treated HaCaT cells. Moreover, cleaved-PARP, cleaved-caspase-3 and cleaved-caspase-9 were all downregulated by emodin. Furthermore, inflammatory factors IL-1b, IL-6, Cox-2 and iNOS were inhibited by emodin in LPS-treated cells. In addition, emodin decreased phosphorylation of p65 and IjBa and the level of PTEN while enhanced phosphorylation of PI3K and AKT. Importantly, emodin increased expression of miR-21 suppressed by LPS and miR-21 downregulation negated the protective functions of emodin. Conclusions: Emodin promoted cell growth presented by increasing viability and blocking apoptosis process with inflammation inhibition. The protective activity of emodin was mediated by miR-21 up-regulation.

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Section: Lps-induced Inflammation Was Alleviated By Emodinmentioning

confidence: 61%

Emodin protects against lipopolysaccharide-induced inflammatory injury in HaCaT cells through upregulation of miR-21

Song

Cui

Zhao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Improper activation of JNK and NF‐κB pathways can promote inflammatory response via up‐regulating the expression of inflammatory factors (Liu & Rondinone, ; Ma & Hottiger, ). Romana et al reported that caffeic acid phenethyl ester promoted wound healing of mice pressure ulcers through activating NF‐κB pathway (Romana‐Souza, Dos Santos, & Monte‐Alto‐Costa, ). In the current research, we found that LPS treatment activated JNK and NF‐κB pathways in HaCaT cells, whereas TAN treatment relieved the LPS‐induced activation of JNK and NF‐κB pathways in HaCaT cells.…”

Section: Discussionmentioning

confidence: 99%

Retracted: Tanshinol relieves lipopolysaccharide‐induced inflammatory injury of HaCaT cells via down‐regulation of microRNA‐122

Wang

Wei²

2019

Phytotherapy Research

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This study investigated the effects of tanshinol (TAN) on lipopolysaccharide (LPS)induced human keratinocytes inflammatory injury and underlying potential molecular mechanisms. Viability and apoptosis of HaCaT cells were assessed using MTT assay and Annexin V-FITC/PI staining, respectively. Quantitative reverse transcription-polymerase chain reaction was performed to measure the expression of microRNA-122 (miR-122) in HaCaT cells. Cell transfection was conducted to up-regulate the expression of miR-122. Western blotting was used to detect the protein expression levels of key factors involved in cell apoptosis, inflammatory response, c-Jun N-terminal kinase (JNK), and nuclear factor kappa B (NF-κB) pathways. We found that LPS treatment induced HaCaT cell inflammatory injury by inhibiting cell viability, promoting cell apoptosis, and enhancing the protein expression levels of cyclooxygenase 2 and inducible nitric oxide synthase. TAN treatment relieved LPS-induced HaCaT cell inflammatory injury. Moreover, TAN treatment attenuated LPS-induced activation of JNK and NF-κB pathways in HaCaT cells. Furthermore, TAN treatment alleviated LPS-induced up-regulation of miR-122. Overexpression of miR-122 reversed the effects of TAN on LPS-induced HaCaT cell inflammatory injury and activation of JNK and NF-κB pathways. In conclusion, TAN exerted anti-inflammatory and protective effects on keratinocytes injury. TAN relieved LPS-induced inflammatory injury of human HaCaT cells via downregulating miR-122 and then inactivating JNK and NF-κB pathways.

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“…Tissue analysis 70 days after the burn also confirmed the long-term effect of CAPE, as it showed a reduced amount of myofibroblasts and CD68 positive macrophages in the CAPE group, and higher levels of hydroxyproline. These data show that the effect of CAPE on burn healing is still visible even after 70 days (CAPE administration stopped 14 days after the burn) [ 62 ]. Attention should be paid to some kind of modulation of proinflammatory mediator expression by CAPE used in wound healing.…”

Section: Biological Propertiesmentioning

confidence: 99%

The Pluripotent Activities of Caffeic Acid Phenethyl Ester

et al. 2021

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Caffeic acid phenethyl ester (CAPE) is a strong antioxidant extracted from honey bee-hive propolis. The mentioned compound, a well-known NF-κB inhibitor, has been used in traditional medicine as a potent anti-inflammatory agent. CAPE has a broad spectrum of biological properties including anti-viral, anti-bacterial, anti-cancer, immunomodulatory, and wound-healing activities. This review characterizes published data about CAPE biological properties and potential therapeutic applications, that can be used in various diseases.

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Caffeic acid phenethyl ester promotes wound healing of mice pressure ulcers affecting NF-κB, NOS2 and NRF2 expression

Cited by 43 publications

References 59 publications

Emodin protects against lipopolysaccharide-induced inflammatory injury in HaCaT cells through upregulation of miR-21

Emodin protects against lipopolysaccharide-induced inflammatory injury in HaCaT cells through upregulation of miR-21

Retracted: Tanshinol relieves lipopolysaccharide‐induced inflammatory injury of HaCaT cells via down‐regulation of microRNA‐122

The Pluripotent Activities of Caffeic Acid Phenethyl Ester

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