Nuclear sirtuins and inflammatory signaling pathways

Mendes, Keila Lopes; Lelis, Deborah de Farias; Santos, Sérgio Henrique Sousa

doi:10.1016/j.cytogfr.2017.11.001

Cited by 200 publications

(133 citation statements)

References 102 publications

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“…However, other prostaglandin‐independent mechanisms may be involved in the actions of diclofenac, for example, activation of potassium channels (K Ca , K v , and K 2P ), the nitric oxide‐cGMP pathway, biguanide‐dependent mechanisms, blockade of proton‐gated ion channels, and NMDA receptors (Gan, ; Ortiz, ; Ortiz et al, , ; Veale et al, ; Voilley, ). In this study, DHA produced antinociception in the 1% rat formalin test via mechanisms of action previously described (Calder, ; Schuchardt & Hahn, ; Mendes et al, ; López‐Vicario et al, ; Oh et al, ; Im, ). Administration of DHA by the intracerebroventricular route reduced formalin‐induced pain behavior possibly via activation of GPR40 and β‐endorphin release (Nakamoto et al, ).…”

Section: Discusionmentioning

confidence: 59%

“…in vivo arachidonic acid (AA)‐derived inflammatory eicosanoid formation is modestly increased by DHA (Calder, ). Nuclear factor κβ (NF‐κβ) is a master transcription factor involved in the expression of inflammatory mediators (Mendes, Lelis, & Santos, ). Its activation can be suppressed by DHA along with activation of the peroxisome proliferator‐activated receptor γ (PPAR γ) and/or the G protein‐coupled receptor 120 (GPR120), a putative ω‐3 PUFA receptor predominantly expressed in inflammatory cells (Oh et al, ).…”

Section: Discusionmentioning

confidence: 99%

“…DHA in food or dietary supplements is absorbed and integrated into the lipid membranes of the cells, which can decrease of AA‐derived inflammatory prostanoids (Calder, ; Schuchardt & Hahn, ). Other anti‐inflammatory mechanisms of DHA involve binding to GPR120 and PPAR γ receptors, to block the NFκß pathway and decreasing proinflammatory mediators including as cytokines, interleukins and adhesion molecules (López‐Vicario et al, ; Mendes et al, ; Oh et al, ).…”

Section: Discusionmentioning

confidence: 99%

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Synergistic interaction between docosahexaenoic acid and diclofenac on inflammation, nociception, and gastric security models in rats

Miranda-Lara

Ortiz

Rodríguez-Ramos

et al. 2018

Drug Development Research

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Preclinical Research & Development The addition of polyunsaturated fatty acids to nonsteroidal anti-inflammatory drugs can increase their antinociceptive activity and produce a gastroprotective effect. The aim of the present study was to examine the effects of the interaction between docosahexaenoic acid (DHA) and diclofenac on inflammation (fixed ratios 1:1, 1:3, and 3:1), nociception (fixed ratio 1:3), and gastric injury in rats. DHA, diclofenac, or combinations of DHA and diclofenac produced anti-inflammatory and antinociceptive effects in rat. The administration of diclofenac produced significant gastric damage, but this effect was not observed with either DHA or the DHA-diclofenac combinations. Effective dose (ED ) values were estimated for each individual drug and analyzed isobolographically. The anti-inflammatory experimental ED values were 6.97 mg/kg (1:1 fixed ratio), 1.1 mg/kg (1:3 fixed ratio), and 11.34 mg/kg (3:1 fixed ratio). These values were significantly lower (p < .05) than the theoretical ED values: 67.94 mg/kg (1:1), 35.37 mg/kg (1:3), and 100.51 mg/kg (3:1). The antinociceptive experimental value was 1.25 mg/kg (1:3 fixed ratio). This value was lower (p < .05) than the theoretical ED , which was predicted to be 15.92 mg/kg. These data indicate that the DHA-diclofenac combinations interact at the systemic level, produce minor gastric damage, and potentially have therapeutic advantages for the clinical treatment of inflammatory pain.

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Section: Discusionmentioning

confidence: 59%

Section: Discusionmentioning

confidence: 99%

Section: Discusionmentioning

confidence: 99%

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Synergistic interaction between docosahexaenoic acid and diclofenac on inflammation, nociception, and gastric security models in rats

Miranda-Lara

Ortiz

Rodríguez-Ramos

et al. 2018

Drug Development Research

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“…Importantly, many effects of SIRT1 that are relevant to the suppression or avoidance of inflammation have been also observed upon treatment with melatonin (Figure ). In addition to the inhibition of NF‐κB activation, to Nrf2 upregulation, and to the avoidance of NLRP3 inflammasome activation, several further anti‐inflammatory actions of SIRT1 have become known. This concerns, for example, an inhibition of TLR4, which was demonstrated in renal collecting duct cells by either SIRT1 overexpression or activation by SRT1720, effects that were blocked by Sirt1 siRNA or the sirtuin inhibitors sirtinol and EX527 .…”

Section: Downstream Factors Of Melatonin's Actions With Relevance To mentioning

confidence: 99%

Melatonin and inflammation—Story of a double‐edged blade

Hardeland

2018

Journal of Pineal Research

343

350

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Melatonin is an immune modulator that displays both pro‐ and anti‐inflammatory properties. Proinflammatory actions, which are well documented by many studies in isolated cells or leukocyte‐derived cell lines, can be assumed to enhance the resistance against pathogens. However, they can be detrimental in autoimmune diseases. Anti‐inflammatory actions are of particular medicinal interest, because they are observed in high‐grade inflammation such as sepsis, ischemia/reperfusion, and brain injury, and also in low‐grade inflammation during aging and in neurodegenerative diseases. The mechanisms contributing to anti‐inflammatory effects are manifold and comprise various pathways of secondary signaling. These include numerous antioxidant effects, downregulation of inducible and inhibition of neuronal NO synthases, downregulation of cyclooxygenase‐2, inhibition of high‐mobility group box‐1 signaling and toll‐like receptor‐4 activation, prevention of inflammasome NLRP3 activation, inhibition of NF‐κB activation and upregulation of nuclear factor erythroid 2‐related factor 2 (Nrf2). These effects are also reflected by downregulation of proinflammatory and upregulation of anti‐inflammatory cytokines. Proinflammatory actions of amyloid‐β peptides are reduced by enhancing α‐secretase and inhibition of β‐ and γ‐secretases. A particular role in melatonin's actions seems to be associated with the upregulation of sirtuin‐1 (SIRT1), which shares various effects known from melatonin and additionally interferes with the signaling by the mechanistic target of rapamycin (mTOR) and Notch, and reduces the expression of the proinflammatory lncRNA‐CCL2. The conclusion on a partial mediation by SIRT1 is supported by repeatedly observed inhibitions of melatonin effects by sirtuin inhibitors or knockdown.

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“…Recently, studies have shown that SIRT1 possesses the ability to inhibit inflammatory response . In the present study, we detected the expression of SIRT1 in TiPs‐treated animal models and macrophages.…”

Section: Resultsmentioning

confidence: 69%

Hydrogen sulfide protects against particle‐induced inflammatory response and osteolysis via SIRT1 pathway in prosthesis loosening

et al. 2020

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Wear debris‐induced osteolysis and ensuing aseptic loosening is the main cause of implant failure and revision surgery. Wear debris‐induced inflammatory response plays key roles in peri‐implant osteolysis. Recently, substantial of evidence suggests that hydrogen sulfide (H2S), the third gasotransmitter, is a critical player regulating inflammation. However, the role and therapeutic potential of H2S in wear debris‐induced inflammation and osteolysis remains to be defined. In the present study, we investigated the effect of H2S on wear debris‐induced pro‐inflammatory cytokines expression and osteolysis in vitro and in vivo. With a slow‐releasing H2S donor GYY4137, our study demonstrated that H2S attenuated wear debris‐induced osteolysis and osteoclastogenesis in murine calvaria resorption models. The expression of tumor necrosis factor‐alpha (TNF‐α), interleukin‐1β (IL‐1β), and interleukin‐6 (IL‐6) that stimulated by wear particles were significantly reduced by GYY4137. Further, the level of sirtuin 1 (SIRT1), which possesses anti‐inflammation property, was examined in vivo and in macrophages. And we found that wear debris decreased the expression of SIRT1. Cotreated macrophages with GYY4137 in part reversed the decline of SIRT1. More importantly, with the SIRT1 recombinant lentivirus and small interfering RNAs (siRNA) against SIRT1, our data indicated that SIRT1 mediated the inhibitory effects of GYY4137 on wear debris‐induced inflammation. Collectively, these results suggested that exogenous H2S production (via H2S donors) may represent a potential approach for the treatment of wear particle‐induced osteolysis.

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Nuclear sirtuins and inflammatory signaling pathways

Cited by 200 publications

References 102 publications

Synergistic interaction between docosahexaenoic acid and diclofenac on inflammation, nociception, and gastric security models in rats

Synergistic interaction between docosahexaenoic acid and diclofenac on inflammation, nociception, and gastric security models in rats

Melatonin and inflammation—Story of a double‐edged blade

Hydrogen sulfide protects against particle‐induced inflammatory response and osteolysis via SIRT1 pathway in prosthesis loosening

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