Dihydromyricetin relieves rheumatoid arthritis symptoms and suppresses expression of pro-inflammatory cytokines via the activation of Nrf2 pathway in rheumatoid arthritis model

Chu, Ji; Wang, Xiujun; Bi, Huanjie; Li, Lifeng; Ren, Mingguang; Wang, Jingwei

doi:10.1016/j.intimp.2018.04.001

Cited by 55 publications

(29 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Abe and Tanaka (37) demonstrated that Nrf2 can attenuate the expression of IL-6 and IL-1β, which decreased the macrophage inflammatory response. The study of Chu et al (38), demonstrated that the expression levels of IL-6, IL-1β and TNF-α are significantly inhibited by SFN in a rheumatoid arthritis model. These results demonstrate that Nrf2 can regulate the downstream cytokines, including IL-6, IL-1β and TNF-α, to influence the progression of inflammation in AD.…”

Section: Discussionmentioning

confidence: 99%

Sulforaphane has a therapeutic effect in an atopic dermatitis murine model and activates the Nrf2/HO‑1 axis

Peng

Yang

et al. 2019

Mol Med Report

View full text Add to dashboard Cite

Atopic dermatitis (AD), a chronic inflammatory skin disease, is characterized by intense itching and recurrent eczematous lesions. Sulforaphane is known to attenuate oxidative stress, and tissue or cell damage in cerebral ischemia, brain inflammation and intracerebral hemorrhage. In the present study, a 2,4-dinitrochlorobenzene (DNCB)-induced AD mouse model was developed, and ear thickness, dermatitis score, eosinophil count, mast cell infiltration, and serum IgE levels were measured in DNCB-induced AD and sulforaphane-treated groups to demonstrate the therapeutic effects of sulforaphane. AD symptoms of DNCB-induced mice were attenuated by sulforaphane treatment compared with those of negative control mice; furthermore, eosinophil count, mast cell infiltration and serum IgE levels were also reduced by sulforaphane treatment in DNCB-induced AD mice. Western blot assays revealed that the expression levels of nuclear factor-E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1), which exhibit oxidation resistance, were increased by sulforaphane treatment in DNCB-induced AD mice. The present study suggested that sulforaphane exerted a therapeutic effect in the AD mouse model through the activation of the Nrf2/HO-1 axis as well as the suppression of Janus kinase 1/STAT3 signaling pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Sulforaphane has a therapeutic effect in an atopic dermatitis murine model and activates the Nrf2/HO‑1 axis

Peng

Yang

et al. 2019

Mol Med Report

View full text Add to dashboard Cite

show abstract

“…Various studies have shown that genetic and environmental risk factors together contribute to the development of RA . An increasing number of studies are identifying a correlation between the cytokine networks and the RA pathogenesis . At present, tremendous achievement has been seen in developing effective treatment of RA, in which suppressing the inflammatory responses is the most effect method .…”

Section: Introductionmentioning

confidence: 99%

“…[3][4][5][6] An increasing number of studies are identifying a correlation between the cytokine networks and the RA pathogenesis. 7,8 At present, tremendous achievement has been seen in developing effective treatment of RA, in which suppressing the inflammatory responses is the most effect method. 5,9,10 However, further studies are necessary to discover the mechanism in inflammatory responses of RA.…”

Section: Introductionmentioning

confidence: 99%

LncRNA MEG3 inhibits rheumatoid arthritis through miR‐141 and inactivation of AKT/mTOR signalling pathway

Liu

Meng

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

Rheumatoid arthritis (RA) is a chronic inflammation mediated by autoimmune responses. MEG3, a kind of long noncoding RNA (lncRNA), participates in cell proliferation in cancer tissues. However, the correlation between MEG3 and RA is yet unclear. Therefore, to clarify how MEG3 works in RA, we performed a series of experiments using RA samples. We found that MEG3 was downregulated in the fibroblast‐like synoviocytes of RA patients (RA‐FLS), in comparison with healthy subjects. MEG3 was also down‐regulated evidently in lipopolysaccharide (LPS)‐treated chondrocyte. As part of our experiments, MEG3 was overexpressed in chondrocyte by transfection with lentivirus containing sequences encoding MEG3. In addition, in presence of LPS, reductions were identified not only in the cell proliferation, but also in the generation of interleukin‐23 (IL‐23), which, however were reversed in the lentivirus (containing MEG3‐encoding sequences)‐transfected chondrocytes. Up‐regulated MEG3 resulted in an increase the level of Ki67. Moreover, MEG3 was negatively correlated with miR‐141, and miR‐141 was up‐regulated in LPS‐treated chondrocyte. Inhibitory effects of MEG3 overexpression, mentioned above, were partially abolished by overexpressed miR‐141. Further, animal experiment also showed the inhibitory effect of MEG3 in overexpression on the AKT/mTOR signaling pathway. In‐vivoexperiments also showed that cell proliferation was facilitated by MEG3 overexpression with inhibited inflammation. In summary, the protective role of MEG3 in RA was proved to be exerted by the increase in the rate of proliferation, which might correlate to the regulatory role of miR‐141 and AKT/mTOR signal pathway, suggesting that MEG3 holds great promise as a therapeutic strategy for RA.

show abstract

“…Therefore, this study has greatly enriched the chemical constituents and diversity. Among them, 15 flavonoids, including procyanidin B2 (peak 9) (Wang et al, 2017b), dihydromyricetin (peak 10) (Chu et al, 2018), (-)-epicatechin (peak 11) (Osman et al, 2019), puerarin (peak 12) (Wang et al, 2016), rutin (peak 24) (Sun et al, 2017), naringin (peak 28) (Ahmad et al, 2014), hesperidin (peak 32) (Li et al, 2019a), myricetin (peak 35) (Yuan et al, 2015), eriodictyol (peak 40) (Lei et al, 2020), quercetin (peak 41) (Saccol et al, 2019), naringenin (peak 43) (Zhu et al, 2015), kaempferol (peak 44) (Pan et al, 2018), diosmetin (peak 46) (Chen et al, 2019), nobiletin (peak 51) (Li et al, 2019a), and tangeretin (peak 53) (Li et al, 2019c), have been reported to have arthritis inhibitory effect in rats. Additionally, cinnamaldehyde (peak 8, phenylpropanoid) (Mateen et al, 2019), ursolic acid (peak 65, triterpenoid) (Kim et al, 2018), linoleic acid (peak 67, fatty acid) (Wang et al, 2011) and emodin (peak 54, other) (Zhu et al, 2013) were also exhibited anti-arthritis activities in vivo.…”

Section: Phytochemicals Identification Of P Heterophyllum Using Ultrmentioning

confidence: 99%

Chemical Composition of Pterospermum heterophyllum Root and its Anti-Arthritis Effect on Adjuvant-Induced Arthritis in Rats via Modulation of Inflammatory Responses

et al. 2020

View full text Add to dashboard Cite

Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease without effective and beneficial drugs. Many traditional folk medicines have been proven to be effective in treating RA. Among these, the root of Pterospermum heterophyllum Hance has been widely used as a traditional remedy against RA in China, but there is no scientific basis yet. The aim of this study was to investigate for the first time the chemical compositions and therapeutic effect of P. heterophyllum on adjuvant-induced arthritis (AIA) model in rats. 73 compounds were identified from P. heterophyllum based on ultra-performance liquid chromatography-quadrupole time-of-flight tandem mass spectrometry (UPLC-qTOF-MS/MS), and flavonoids may be partly responsible for the major anti-arthritic effect. In parallel, the P. heterophyllum extract at 160, 320, and 640 mg/kg/day were orally administered to rats for 22 days after post-administration adjuvant. The results showed that P. heterophyllum remarkably ameliorated histological lesions of the knee joint, increased body weight growth, decreased arthritis score, reduced thymus and spleen indices in model rats. Moreover, P. heterophyllum treatment persuasively downregulated the levels of rheumatoid factor (RF), C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), IL-6, IL-17, cyclooxygenase-2 (COX-2), 5-lipoxygenase (5-LOX) and matrix metalloproteinase-2 (MMP-2), and observably upregulated IL-4 and IL-10 levels in model rats. These findings suggest that P. heterophyllum has a prominent anti-RA effect on AIA rats by modulating the inflammatory responses, and supports the traditional folk use of this plant.

show abstract

Dihydromyricetin relieves rheumatoid arthritis symptoms and suppresses expression of pro-inflammatory cytokines via the activation of Nrf2 pathway in rheumatoid arthritis model

Cited by 55 publications

References 30 publications

Sulforaphane has a therapeutic effect in an atopic dermatitis murine model and activates the Nrf2/HO‑1 axis

Sulforaphane has a therapeutic effect in an atopic dermatitis murine model and activates the Nrf2/HO‑1 axis

LncRNA MEG3 inhibits rheumatoid arthritis through miR‐141 and inactivation of AKT/mTOR signalling pathway

Chemical Composition of Pterospermum heterophyllum Root and its Anti-Arthritis Effect on Adjuvant-Induced Arthritis in Rats via Modulation of Inflammatory Responses

Contact Info

Product

Resources

About