Anti-inflammatory activity of myricetin from <i>Diospyros lotus</i> through suppression of NF-κB and STAT1 activation and Nrf2-mediated HO-1 induction in lipopolysaccharide-stimulated RAW264.7 macrophages

Cho, Byoung Ok; Yin, Hong; Park, Sang Hyun; Byun, Eui Baek; Ha, Hun Yong; Jang, Seon Il

doi:10.1080/09168451.2016.1171697

Cited by 104 publications

(56 citation statements)

References 37 publications

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“…Further investigation revealed that the activity of NF- κ B was much higher in Nrf2 −/− mice than in their wild-type counterparts [21]. In LPS-stimulated RAW264.7 macrophages, M treatment suppressed the production of NO, iNOS, TNF- α , IL-6, and IL-12 by depressing the activity of NF- κ B and the degradation of I κ B- α via promoting Nrf2/HO-1 pathway [22]. Our study indicated that silencing of Nrf2 could further activate the phosphorylation of I κ B- α /NF- κ B/p65 signaling in NRCM after incubation with high glucose for 72 h. We also detected further overexpression of IL-1 β , IL-6, and TNF- α at mRNA level after Nrf2 silencing by stimulating with LPS for 16 h. These results were coincident with previous reports that Nrf2 could inhibit I κ B- α /NF- κ B/p65 signaling.…”

Section: Discussionmentioning

confidence: 99%

Myricetin Possesses Potential Protective Effects on Diabetic Cardiomyopathy through Inhibiting IκBα/NFκB and Enhancing Nrf2/HO‐1

Liao

Zhu

Hong

et al. 2017

Oxidative Medicine and Cellular Longevity

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Diabetic cardiomyopathy (DCM) is associated with a greater risk of mortality in patients with diabetes mellitus. Currently, no specific treatment has been suggested for DCM treatment. This study demonstrated that myricetin (M) attenuated DCM-associated cardiac injury in mice subjected to streptozotocin (SZT) and in neonatal rat cardiomyocytes (NRCM) challenged with high glucose. In vivo investigation demonstrated 6 months of M treatment (200 mg/kg/d) significantly alleviated cardiac hypertrophy, apoptosis, and interstitial fibrosis. Mechanically, M treatment significantly increased the activity of Nrf2/HO-1 pathway, strengthening antioxidative stress capacity evidenced by reversed activities of GPx and SOD, and decreased MDA production. M treatment also inhibited IκBα/NF-κB pathway, resulting in reduced secretion of inflammation cytokines including IL-1β, TNF-α, and IL-6. Besides, the TGFβ/Smad3 signaling was also blunted in DCM mice treated with M. These beneficial effects of M treatment protected cardiomyocytes from apoptosis as shown by decreased TUNEL-positive nucleus, c-caspase 3, and Bax. Similar effects of M treatment could be reproduced in NRCM treated with high glucose. Furthermore, through silencing Nrf2 in NRCM, we found that the regulation of IκBα/NFκB by M was independent on its function on Nrf2. Thus, we concluded that M possesses potential protective effects on DCM through inhibiting IκBα/NFκB and enhancing Nrf2/HO-1.

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Section: Discussionmentioning

confidence: 99%

Myricetin Possesses Potential Protective Effects on Diabetic Cardiomyopathy through Inhibiting IκBα/NFκB and Enhancing Nrf2/HO‐1

Liao

Zhu

Hong

et al. 2017

Oxidative Medicine and Cellular Longevity

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“…In previous studies, myricetin has been showed to protect the mouse or rat heart from isoproterenol induced myocardial infarction(Tiwari, Mohan, Kasture, Maxia, & Ballero, ), ischemia/reperfusion induced injury (Scarabelli et al, ), and hypertension (Borde, Mohan, & Kasture, ), and the underlying mechanism was related to the regulation of Stat1 and oxidative stress (Borde et al, ; Scarabelli et al, ; Tiwari et al, ). In in vitro experiments, myricetin could blunt the activation of NF‐κB and inhibit the production of proinflammatory cytokines in H9C2 cardiomyocytes (Chen & Fan, ) and macrophages (Cho et al, ). Our data confirmed the role of myricetin in antagonizing LPS induced inflammatory response in NRCM and macrophage.…”

Section: Discussionmentioning

confidence: 99%

“…In H9c2 cardiomyocytes, myricetin mitigated the inflammatory responses induced by LPS through regulation of oxidative stress and IκB/NFκB (p65) signaling pathway (Chen & Fan, ). In macrophage, myricetin inhibited the production of inflammatory cytokines by suppressing the activity of NFκB and STAT1 (Cho et al, ). These in vitro experiments have implied the potential benefits of myricetin in SIMD treatment.…”

Section: Introductionmentioning

confidence: 99%

Myricetin attenuated LPS induced cardiac injury in vivo and in vitro

Zhang

Hong

Liao

et al. 2017

Phytotherapy Research

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Sepsis induced myocardial dysfunction (SIMD) is a common complication and leads to an increased mortality. SIMD is closely related to inflammation and oxidative stress. Myricetin exhibits strong capacities of anti-inflammation and anti-oxidative stress, but its pharmacological effects for lipopolysaccharide (LPS) induced cardiac injury remains undefined. This study aimed to explore whether myricetin was efficient to alleviate SIMD in mice and neonatal rat cardiomyocytes injury. Mice administrated with myricetin (100 mg/kg, po, bid) or vehicle groups were challenged with LPS (10 mg/kg, ip), and cardiac functions examined by echocardiography after 12 hr LPS exposure. LPS markedly impaired mouse cardiac functions, which were significantly attenuated by myricetin administration. Myricetin significantly reduced the production of inflammatory cytokines both in serum and cardiac tissue. Myricetin could inhibit the nuclear translocation of p65, degradation of IκBα, and cellular apoptosis in vivo and in vitro. Myricetin also prevented overexpression of iNOS and reduction of oxidoreductase (SOD and GPx) activity. Besides, Myricetin treatment could attenuate production of inflammatory cytokines of peritoneal macrophages stimulated with LPS in vitro. Thus we concluded that myricetin could attenuate the LPS induced cardiac inflammation injury in vivo and in vitro. Myricetin may be a potential therapy or adjuvant therapy for SIMD.

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“…Morin treatment prior to H 2 O 2 exposure significantly prevented the generation of ROS, increased cell viability and prevented DNA damage by up-regulating Nrf2-dependent HO-1 expression through extracellular signal-regulated kinases (ERK) in C2C12 myoblasts [133]. In the case of myricetin, production of pro-inflammatory mediators through the suppression of signal transducer and activator of transcription 1 (STAT1) and Nuclear factor kappa-lightchain-enhancer of B cells (NF-kB) activation was inhibited by induction of Nrf2-mediated HO-1 expression in LPS-stimulated macrophages [134].…”

Section: Modulation Of Nrf2 Activity By Phenolic Compoundsmentioning

confidence: 99%

Impact of Antioxidant Natural Compounds on the Thyroid Gland and Implication of the Keap1/Nrf2 Signaling Pathway

Paunkov

Chartoumpekis

Ziros

et al. 2019

CPD

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Background: Natural compounds with potential antioxidant properties have been used in the form of food supplements or extracts with the intent to prevent or treat various diseases. Many of these compounds can activate the cytoprotective Nrf2 pathway. Besides, some of them are known to impact the thyroid gland, often with potential side-effects, but in other instances, with potential utility in the treatment of thyroid disorders. Objective: In view of recent data regarding the multiple roles of Nrf2 in the thyroid, this review summarizes the current bibliography on natural compounds that can have an effect on thyroid gland physiology and pathophysiology, and it discusses the potential implication of the Nrf2 system in the respective mechanisms. Method & Results: Literature searches for articles from 1950 to 2018 were performed in PubMed and Google Scholar using relevant keywords about phytochemicals, Nrf2 and thyroid. Natural substances were categorized into phenolic compounds, sulfur-containing compounds, quinones, terpenoids, or under the general category of plant extracts. For individual compounds in each category, respective data were summarized, as derived from in vitro (cell lines), preclinical (animal models) and clinical studies. The main emerging themes were as follows: phenolic compounds often showed potential to affect the production of thyroid hormones; sulfur-containing compounds impacted the pathogenesis of goiter and the proliferation of thyroid cancer cells; while quinones and terpenoids modified Nrf2 signaling in thyroid cell lines. Conclusion: Natural compounds that modify the activity of the Nrf2 pathway should be evaluated carefully, not only for their potential to be used as therapeutic agents for thyroid disorders, but also for their thyroidal safety when used for the prevention and treatment of non-thyroidal diseases.

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Anti-inflammatory activity of myricetin from Diospyros lotus through suppression of NF-κB and STAT1 activation and Nrf2-mediated HO-1 induction in lipopolysaccharide-stimulated RAW264.7 macrophages

Cited by 104 publications

References 37 publications

Myricetin Possesses Potential Protective Effects on Diabetic Cardiomyopathy through Inhibiting IκBα/NFκB and Enhancing Nrf2/HO‐1

Myricetin Possesses Potential Protective Effects on Diabetic Cardiomyopathy through Inhibiting IκBα/NFκB and Enhancing Nrf2/HO‐1

Myricetin attenuated LPS induced cardiac injury in vivo and in vitro

Impact of Antioxidant Natural Compounds on the Thyroid Gland and Implication of the Keap1/Nrf2 Signaling Pathway

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