Effect of caffeic acid phenethyl ester on <i><scp>P</scp>revotella intermedia</i> lipopolysaccharide‐induced production of proinflammatory mediators in murine macrophages

Choi, Eun‐Young; Choe, So-Hui; Hyeon, Jin-Yi; Choi, Jaeho; Choi, In-soon; Kim, S.-J.

doi:10.1111/jre.12260

Cited by 28 publications

(22 citation statements)

References 57 publications

(77 reference statements)

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“…3 In preclinical models, CAPE protected against ligature-induced periodontitis 4 and systemic bone loss by cortisone, 5 and supported bone defect healing. 6 Therefore, CAPE is attracting attention in periodontology, 7,8 and interest is growing in uncovering the beneficial effects of CAPE in periodontal therapy.…”

Section: Introductionmentioning

confidence: 99%

“…For example, CAPE prevents damage of cells exposed to hydrogen peroxide, including neurite PC12 cells, 12 retinal 661W cells 13 and umbilical vein endothelial cells. 14 CAPE also exerts anti-inflammatory activity in gingival fibroblasts 7 and macrophages 8 exposed to endotoxins. Thus, CAPE supports the major defence mechanisms of cells challenged by oxidative stress and inflammation.…”

Section: Introductionmentioning

confidence: 99%

“…For instance, CAPE increases HO1 expression in gingival fibroblasts 7 and macrophages. 8 In turn, HO1 activates the cellular defence mechanisms against oxidative stress, 19 including superoxide dismutase (SOD), catalase (CAT) and glutathione S -transferase (GST) expression. 20 In support of this mechanism, Nrf2 21 and HO1 22,23 regulate SOD expression.…”

Section: Introductionmentioning

confidence: 99%

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Caffeic acid phenethyl ester protects against oxidative stress and dampens inflammation via heme oxygenase 1

et al. 2019

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Periodontal disease is associated with chronic oxidative stress and inflammation. Caffeic acid phenethyl ester (CAPE), which is a potent inducer of heme oxygenase 1 (HO1), is a central active component of propolis, and the application of propolis improves periodontal status in diabetic patients. Here, primary murine macrophages were exposed to CAPE. Target gene expression was assessed by whole-genome microarray, RT-PCR and Western blotting. The antioxidative and anti-inflammatory activities of CAPE were examined by exposure of the cells to hydrogen peroxide, saliva and periodontal pathogens. The involvement of HO1 was investigated with the HO1 inhibitor tin protoporphyrin (SnPP) and knockout mice for Nrf2, which is a transcription factor for detoxifying enzymes. CAPE increased HO1 and other heat shock proteins in murine macrophages. A p38 MAPK inhibitor and Nrf2 knockout attenuated CAPE-induced HO1 expression in macrophages. CAPE exerted strong antioxidative activity. Additionally, CAPE reduced the inflammatory response to saliva and periodontal pathogens. Blocking HO1 decreased the antioxidative activity and attenuated the anti-inflammatory activity of CAPE. In conclusion, CAPE exerted its antioxidative effects through the Nrf2-mediated HO1 pathway and its anti-inflammatory effects through NF-κB inhibition. However, preclinical models evaluating the use of CAPE in periodontal inflammation are necessary in future studies.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Caffeic acid phenethyl ester protects against oxidative stress and dampens inflammation via heme oxygenase 1

et al. 2019

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“…Increasing evidence has indicated that different mechanisms are involved in the various functions of CAPE, including induction of HO-1 expression, activation of the ERK1/2-CREB signalling cascade and inhibition of NF-κB signals in different cell contexts and different disease models [ 42 – 45 ]. We found that CAPE upregulated the HIF-1α and SDF-1α gene and protein expression in BMECs, which further supports the hypothesis that CAPE has the ability to improve haematopoietic cell homing by regulating the BM niche (Fig.…”

Section: Discussionmentioning

confidence: 99%

Caffeic acid phenethyl ester promotes haematopoietic stem/progenitor cell homing and engraftment

Chen

Han²,

Zhang³

et al. 2017

Stem Cell Res Ther

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BackgroundSeveral studies have suggested that caffeic acid phenethyl ester (CAPE) can induce the expression of hypoxia inducible factor-1α (HIF-1α) protein. We determined whether CAPE has a novel function in improving the homing and engraftment of haematopoietic stem/progenitor cells (HSPCs) by regulating HIF-1α gene expression in the bone marrow (BM) niche.MethodsFor survival experiments, lethally irradiated C57BL/6 mice were injected with a low number of BM mononuclear cells (MNCs) and CAPE according to the indicated schedule. Homing efficiency analysis was conducted using flow cytometry and colony-forming unit (CFU) assays. The influence of intraperitoneal injection of CAPE on short-term and long-term engraftment of HSPCs was evaluated using competitive and non-competitive mouse transplantation models. To investigate the mechanism by which CAPE enhanced HSPC homing, we performed these experiments including Q-PCR, western blot, immunohistochemistry and CFU assays after in-vivo HIF-1α activity blockade.ResultsCAPE injection significantly increased the survival rate of recipient mice after lethal irradiation and transplantation of a low number of BM MNCs. Using HSPC homing assays, we found that CAPE notably increased donor HSPC homing to recipient BM. The subsequent short-term and long-term engraftment of transplanted HSPCs was also improved by the optimal schedule of CAPE administration. Mechanistically, we found that CAPE upregulated the expression of HIF-1α, vascular endothelial growth factor-A (VEGF-A) and stromal cell-derived factor 1α (SDF-1α). The HIF-1α inhibitor PX-478 blocked CAPE-enhanced HSPC homing, which supported the idea that HIF-1α is a key target of CAPE.ConclusionsOur results showed that CAPE administration facilitated HSPC homing and engraftment, and this effect was primarily dependent on HIF-1α activation and upregulation of SDF-1α and VEGF-A expression in the BM niche.Electronic supplementary materialThe online version of this article (doi:10.1186/s13287-017-0708-x) contains supplementary material, which is available to authorized users.

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“…Caffeic acid phenethyl ester (CAPE) has antioxidant, antitumoral, anti-inflammatory, and immunomodulatory properties and inhibits ROS production during inflammatory processes [59]. Recently, it has been reported that CAPE can modulate the host response [60]. Yiğit et al [19] evaluated the effects of LDD and CAPE on alveolar bone level and the plasma levels of GSH-Px activity in an experimental periodontitis rat model.…”

Section: Glutathione Peroxidase Medication and Periodontal Diseasementioning

confidence: 99%

Periodontal Health and Disease in Glutathione Peroxidase

Dede¹

2020

Glutathione System and Oxidative Stress in Health and Disease

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Periodontal diseases are chronic, multifactorial inflammatory diseases that affect more than 10% of the world population. There are two general forms of periodontal diseases including gingivitis (reversible inflammation and confined with gingiva form) and periodontitis (irreversible, destruction form). Several studies have reported that periodontal disease was associated with a decreased antioxidant capacity and elevated oxidative damage within the oral cavity. Glutathione peroxidase (GSH-Px) is an important enzymatic antioxidant that protects periodontal tissues against oxidative stress. Hitherto, there is contradictory evidence concerning the relationship between the levels of GSH-Px and the periodontal status. Various studies have demonstrated that GSH-Px levels in different biological fluids increased, decreased, or are unaltered in individuals with periodontal disease. This discrepancy might be explained either by different determination protocols/assays applied among the studies or various dynamic processes of the periodontal disease progression. In this section, GSH-Px levels are summarized in the periodontal health and disease including the presence and absence of systemic disease, medication, wound healing, and smoking.

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Effect of caffeic acid phenethyl ester on Prevotella intermedia lipopolysaccharide‐induced production of proinflammatory mediators in murine macrophages

Abstract: Modulation of host response by CAPE may represent an attractive strategy towards the treatment of periodontal disease. In vivo studies are required to appraise the potential of CAPE further as an immunomodulator in the treatment of periodontal disease.

Cited by 28 publications

References 57 publications

Caffeic acid phenethyl ester protects against oxidative stress and dampens inflammation via heme oxygenase 1

Caffeic acid phenethyl ester protects against oxidative stress and dampens inflammation via heme oxygenase 1

Caffeic acid phenethyl ester promotes haematopoietic stem/progenitor cell homing and engraftment

Periodontal Health and Disease in Glutathione Peroxidase

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