scholarly journals Fast Green FCF Alleviates Pain Hypersensitivity and Down-Regulates the Levels of Spinal P2X4 Expression and Pro-inflammatory Cytokines in a Rodent Inflammatory Pain Model

2018 ◽  
Vol 9 ◽  
Author(s):  
Fang Xu ◽  
Jing Yang ◽  
Fan Lu ◽  
Rongjun Liu ◽  
Jinwei Zheng ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Inflammatory Pain ◽  
Fast Green ◽  
Pain Model ◽  
Pain Hypersensitivity ◽  
Fast Green Fcf ◽  
Pro Inflammatory Cytokines

scholarly journals Intravenous administration of triptonide attenuates CFA-induced pain hypersensitivity through inhibiting AKT signaling pathway in mice

2020 ◽  
Author(s):  
Yue-Juan Ling ◽  
Ting-Yu Ding ◽  
Yong-Jing Gao ◽  
Bao-Chun Jiang
Keyword(s):  
Inflammatory Cytokines ◽  
Inflammatory Pain ◽  
Mechanical Allodynia ◽  
Interleukin 1 ◽  
Thermal Hyperalgesia ◽  
Paw Edema ◽  
Akt Inhibitor ◽  
Pain Hypersensitivity ◽  
Chronic Inflammatory Pain ◽  
Pro Inflammatory Cytokines

Abstract Background: Triptonide (TPN) is a major component of Tripterygium wilfordii Hook.f., and reportedly has anti-inflammatory and neuroprotective effects. Recent studies have demonstrated that the phosphatidylinositol 3-kinase (PI3K)/AKT pathway plays an important role in the pathogenesis of inflammatory pain. Here we investigated the anti-nociceptive effect of systemic treatment with TPN on mouse models of chronic inflammatory pain and explored possible mechanisms. Results: Unilateral hind paw injection of complete Freund’s adjuvant (CFA) induced paw edema and persistent pain hypersensitivity. Intravenous treatment with TPN attenuated CFA-induced paw edema, mechanical allodynia, and thermal hyperalgesia. Western blotting and immunofluorescence results showed that CFA induced AKT activation in the dorsal root ganglion (DRG) neurons, which was inhibited by TPN treatment. Furthermore, TPN treatment inhibited mRNA increase of proinflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin 1 beta (IL-1β), and Interleukin 6 (IL-6)] induced by CFA. Finally, pretreatment with AKT inhibitor, AKT inhibitor Ⅳ, attenuated CFA-induced mechanical allodynia and thermal hyperalgesia, and decreased the mRNA expression of pro-inflammatory cytokines. Conclusions: These data indicate that TPN attenuates CFA-induced pain potentially via inhibiting AKT-mediated pro-inflammatory cytokines production in DRG. TPN may be used for the treatment of chronic inflammatory pain.

Pro-inflammatory cytokines involvement in the hesperidin antihyperalgesic effects at peripheral and central levels in a neuropathic pain model

2017 ◽  
Vol 25 (2) ◽  
pp. 265-269 ◽  
Author(s):  
A. I. Carballo-Villalobos ◽  
M. E. González-Trujano ◽  
N. Alvarado-Vázquez ◽  
F. J. López-Muñoz
Keyword(s):  
Neuropathic Pain ◽  
Inflammatory Cytokines ◽  
Pain Model ◽  
Neuropathic Pain Model ◽  
Pro Inflammatory Cytokines

scholarly journals Erythronium japonicum Alleviates Inflammatory Pain by Inhibiting MAPK Activation and by Suppressing NF-κB Activation via ERK/Nrf2/HO-1 Signaling Pathway

Antioxidants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 626 ◽  
Author(s):  
Joon Park ◽  
Yun Tai Kim
Keyword(s):  
Protein Kinase ◽  
Inflammatory Cytokines ◽  
Calcium Binding ◽  
Inflammatory Pain ◽  
Microglial Activation ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Cox 2 ◽  
Erythronium Japonicum ◽  
Pro Inflammatory Cytokines

Microglial activation-mediated neuroinflammation influences the development of inflammatory pain. The aim of this study was to investigate the anti-inflammatory effects and mechanisms of aqueous Erythronium japonicum extract (EJE) in microglia activation-mediated inflammatory pain. EJE was found to suppress lipopolysaccharide (LPS)-induced inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), ionized calcium-binding adapter molecule 1 (IBA-1), and pro-inflammatory cytokines in BV2 microglial cells. In addition, LPS-induced c-Jun NH2 terminal protein kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) phosphorylation were inhibited by EJE. Intriguingly, EJE also inhibited p65 phosphorylation by activating extracellular signal-regulated kinase-1/2 (ERK)/nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling. Furthermore, the effects of EJE treatment, such as HO-1 induction and the reduction of NF-ĸB activation, were reversed by ERK1/2 inhibition. In an inflammatory pain mouse model, Complete Freund’s Adjuvant (CFA)-induced mechanical allodynia and foot swelling were alleviated by the oral administration of EJE. Consistent with in vitro results, EJE increased HO-1, while decreasing CFA-induced COX-2, IBA-1, and pro-inflammatory cytokines in the spinal cord. Among the components of EJE, butanol most heavily suppressed LPS-induced microglial activation and increased HO-1 expression. These findings indicate that EJE can alleviate inflammatory pain by inhibiting p38 and JNK and by suppressing NF-ĸB via ERK/Nrf2/HO-1 signaling.

Cytokine synergy, collagenases and cartilage collagen breakdown

2003 ◽  
Vol 70 ◽  
pp. 125-133 ◽  
Author(s):  
Tim E. Cawston ◽  
Jenny M. Milner ◽  
Jon B. Catterall ◽  
Andrew D. Rowan
Keyword(s):  
Matrix Metalloproteinases ◽  
Inflammatory Cytokines ◽  
Activator Protein 1 ◽  
Activator Protein ◽  
And Cartilage ◽  
Pro Inflammatory Cytokines

We have investigated proteinases that degrade cartilage collagen. We show that pro-inflammatory cytokines act synergistically with oncastatin M to promote cartilage collagen resorption by the up-regulation and activation of matrix metalloproteinases (MMPs). The precise mechanisms are not known, but involve the up-regulation of c-fos, which binds to MMP promoters at a proximal activator protein-1 (AP-1) site. This markedly up-regulates transcription and leads to higher levels of active MMP proteins.

Sign in / Sign up

Export Citation Format

Share Document