Resveratrol treatment reveals a novel role for HMGB1 in regulation of the type 1 interferon response in dengue virus infection

Zainal, Nurhafiza; Chang, Chih Peng; Cheng, Yi Lin; Wu, Yang‐Chang; Anderson, Robert; Wan, Shu; Chen, Chia Ling; Ho, Tzong Shiann; AbuBakar, Sazaly; Lin, Yee Shin

doi:10.1038/srep42998

Cited by 54 publications

(50 citation statements)

References 34 publications

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“…Consistent with our findings, pharmacological activation of SIRT1 by resveratrol significantly reduces the extracellular release of HMGB1 (Yu et al, 2019;Zainal et al, 2017) . Accordingly, LDN emerges as an activator of SIRT1 can be explored further to ameliorate the inflammation-induced diseases by decreasing the extracellular level of HMGB1.…”

Section: Discussionsupporting

confidence: 92%

Hyperinsulinemia promotes HMGB1 release leading to inflammation induced systemic insulin resistance: An interplay between pancreatic beta-cell and peripheral organs

Choubey

Kar

Girdhar

et al. 2019

Preprint

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Insulin resistance results from several pathophysiologic mechanisms, including chronic tissue inflammation and defective insulin signaling. Pancreatic β-cells hypersecretion (hyperinsulinemia), is a central hallmark of peripheral insulin resistance. However, the underlying mechanism by which hyperinsulinemia perpetuates towards the development of insulin resistance remains unclear and is still a bigger therapeutic challenge. Here, we found hyperinsulinemia triggers inflammation and insulin resistance by stimulating TLR4-driven inflammatory cascades. We show that hyperinsulinemia activates the TLR4 signaling through HMGB1, an endogenous TLR4 ligand emanating from hyperinsulinemia exposed immune cells and peripheral organs like adipose tissue and liver. Further, our observation suggests hyperinsulinemia ensuring hyperacetylation, nuclear-to-cytoplasmic shuttling and release of HMGB1 into the extracellular space.HMGB1 was also found to be elevated in serum of T2DM patients. We found that extracellular HMGB1 plays a crucial role to promote proinflammatory responses and provokes systemic insulin resistance.Importantly, in-vitro and in-vivo treatment with naltrexone, a TLR4 antagonist led to an anti-inflammatory phenotype with protection from hyperinsulinemia mediated insulin resistance. In-vitro treatment with naltrexone directly enhanced SIRT1 activity, blocked the release of HMGB1 into extracellular milieu, suppressed release of proinflammatory cytokines and ultimately led to insulin-sensitizing effects. These observations elucidate a regulatory network between pancreatic β-cells, macrophage and hepatocytes and assign an unexpected role of TLR4 -HMGB1 signaling axis in hyperinsulinemia mediated systemic insulin resistance.

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Section: Discussionsupporting

confidence: 92%

Hyperinsulinemia promotes HMGB1 release leading to inflammation induced systemic insulin resistance: An interplay between pancreatic beta-cell and peripheral organs

Choubey

Kar

Girdhar

et al. 2019

Preprint

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“…Besides, galloylglucoside derivatives of resveratrol have not been reported before in the genus Terminalia . Resveratrol and its derivatives are antifungal phytoalexins, protecting plants from pathogenic fungal and bacterial intrusion [ 76 , 77 ]. Several investigations on in vitro antifungal activities of resveratrol and its derivatives indicate good antifungal potential of this compound class [ 78 , 79 ].…”

Section: Discussionmentioning

confidence: 99%

LC-MS/MS Tandem Mass Spectrometry for Analysis of Phenolic Compounds and Pentacyclic Triterpenes in Antifungal Extracts of Terminalia brownii (Fresen)

et al. 2017

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Decoctions and macerations of the stem bark and wood of Terminalia brownii Fresen. are used in traditional medicine for fungal infections and as fungicides on field crops and in traditional granaries in Sudan. In addition, T. brownii water extracts are commonly used as sprays for protecting wooden houses and furniture. Therefore, using agar disc diffusion and macrodilution methods, eight extracts of various polarities from the stem wood and bark were screened for their growth-inhibitory effects against filamentous fungi commonly causing fruit, vegetable, grain and wood decay, as well as infections in the immunocompromised host. Ethyl acetate extracts of the stem wood and bark gave the best antifungal activities, with MIC values of 250 µg/mL against Nattrassia mangiferae and Fusarium verticillioides, and 500 µg/mL against Aspergillus niger and Aspergillus flavus. Aqueous extracts gave almost as potent effects as the ethyl acetate extracts against the Aspergillus and Fusarium strains, and were slightly more active than the ethyl acetate extracts against Nattrassia mangiferae. Thin layer chromatography, RP-HPLC-DAD and tandem mass spectrometry (LC-MS/MS), were employed to identify the chemical constituents in the ethyl acetate fractions of the stem bark and wood. The stem bark and wood were found to have a similar qualitative composition of polyphenols and triterpenoids, but differed quantitatively from each other. The stilbene derivatives, cis- (3) and trans- resveratrol-3-O-β-galloylglucoside (4), were identified for the first time in T. brownii. Moreover, methyl-(S)-flavogallonate (5), quercetin-7-β-O-di-glucoside (8), quercetin-7-O-galloyl-glucoside (10), naringenin-4′-methoxy-7-pyranoside (7), 5,6-dihydroxy-3′,4′,7-tri-methoxy flavone (12), gallagic acid dilactone (terminalin) (6), a corilagin derivative (9) and two oleanane type triterpenoids (1) and (2) were characterized. The flavonoids, a corilagin derivative and terminalin, have not been identified before in T. brownii. We reported earlier on the occurrence of methyl-S-flavogallonate and its isomer in the roots of T. brownii, but this is the first report on their occurrence in the stem wood as well. Our results justify the traditional uses of macerations and decoctions of T. brownii stem wood and bark for crop and wood protection and demonstrate that standardized extracts could have uses for the eco-friendly control of plant pathogenic fungi in African agroforestry systems. Likewise, our results justify the traditional uses of these preparations for the treatment of skin infections caused by filamentous fungi.

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“…Studies have shown that the translocation of HMGB1 out of the nucleus is initiated by it acetylation resulting in its relocation. Advance studies have proven that HMGB1 after translocation in the cytoplasm binds to receptors like toll-like receptor 2 (TLR2), TLR4 or receptor for advanced glycation end products (RAGE), resulting the stimulation of numerous complexes of inflammatory responses (104,107,168). Studies have demonstrated RSV blocks HMGB1 translocation out of the nucleus, via the stimulation of sirtuin 1 (Sirt1), a NA-D + -dependent class III protein deacetylase (78,162,168).…”

Section: Resveratrol and Hmgb1 In Gliomamentioning

confidence: 99%

“…Advance studies have proven that HMGB1 after translocation in the cytoplasm binds to receptors like toll-like receptor 2 (TLR2), TLR4 or receptor for advanced glycation end products (RAGE), resulting the stimulation of numerous complexes of inflammatory responses (104,107,168). Studies have demonstrated RSV blocks HMGB1 translocation out of the nucleus, via the stimulation of sirtuin 1 (Sirt1), a NA-D + -dependent class III protein deacetylase (78,162,168). Nevertheless, deacetylation of HMGB1, which results in it detention in the nucleus, is averted when Sirt1 protein interacts with numerous lysine residues at NLS location of HMGB126.…”

Section: Resveratrol and Hmgb1 In Gliomamentioning

confidence: 99%

The Therapeutic Potential of Resveratrol in Gliomas

Richard¹

2019

ABCMed

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Resveratrol (RSV) is found in most human foods especially fruits such as grapes, peanuts, strawberry, blueberry, cranberry, mulberry, lingberry, sparkleberry, bilberry and in flowers as well as leaves like butterfly orchid tree, eucalyptus, spruce, lily, gnetum and so many others. Functionally, RSV has the propensity to safeguard DNA as well as the induction of DNA repair. RSV is precipitously metabolized in the liver via phase-II detoxification enzymes leading to its principal urine excretion. RSV steered growth inhibition, induction of apoptosis and G0/G1phase cell cycle arrest in an experiment involving glioma cells. RVS can block the triggering of signal transducer and activator of transcription (STAT3) signaling of glioma cells. RSV subdues STAT3 signaling via the inhibition of SRC or Janus kinase (JAK2) induction, thereby inducing growth inhibitory and apoptotic properties. RSV explicitly blocks both COX-1 and COX-2 invitro. In the cancer inflammatory milieu, the blockade effects of RSV on NF-κB could also lead to the blockade of TNF-α resulting in inhibition of cancer advancement as well as metastasis.Individually, RSV has proven to very potent in glioma cells. It is able to down-regulate glioma angiogenesis as well as metastasis. In combination with other agents, RVS augment its potency in glioma. RVS is able to cross the blood brain barrier (BBB) via gap junctions making it very efficient central nervous system medication. RVS after oral administration peaks in the blood stream after one hour meaning it acts very fast. This review focuses on the neuropharmacological role of RVS in glioma.proven to have chemo-preventive effects on numerous human ailments like osteoporosis and gastric ulcers besides the cardioprotective effect mentioned above (27,32). STRUCTURE AND FUNCTIONS OF RESVERATROLRSV is a white powder with a feeble yellow cast. It is a stilbene with a natural polyphenol configuration analogous to diethylstilbestrol and estradiol (32,86). Its molecular formula is C 14 H 12 O 3 and it is commonly referred to as 3,5,4'thihydroxystilbene. Other unconventional terms use to describe this compound are: 3,4',5-stilbenetriol, (E)-5-(7-hydroxystyryl) resorcinol, (E)-5-(4-hydroxystyryl) benzene-1,3-diol. RSV occurs innately as both cis-and trans-isomers. The trans-isomer is often used in classic laboratory studies because its more physical available have has higher biological activity than the cis-isomer. On the other hand, the cis-isomer is unstably and not commercial accessible (32,144).Functionally, RSV has the propensity to safeguard DNA as well as the induction of DNA repair (17,89). Studies have proven that, at high dose, RSV does not only suppress cancer advancement but also inhibits the synthesis of RNA, DNA and

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Resveratrol treatment reveals a novel role for HMGB1 in regulation of the type 1 interferon response in dengue virus infection

Cited by 54 publications

References 34 publications

Hyperinsulinemia promotes HMGB1 release leading to inflammation induced systemic insulin resistance: An interplay between pancreatic beta-cell and peripheral organs

Hyperinsulinemia promotes HMGB1 release leading to inflammation induced systemic insulin resistance: An interplay between pancreatic beta-cell and peripheral organs

LC-MS/MS Tandem Mass Spectrometry for Analysis of Phenolic Compounds and Pentacyclic Triterpenes in Antifungal Extracts of Terminalia brownii (Fresen)

The Therapeutic Potential of Resveratrol in Gliomas

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