Suppression of Inflammation and Arthritis by Orally Administrated Cardiotoxin from<i>Naja naja atra</i>

Chen, Cao-Xin; Jie-yu, Chen; Kou, Jianqun; Xu, Yiquan; Wang, Shuzhi; Zhu, Qi; Yang, Lu; Qin, Zheng‐Hong

doi:10.1155/2015/387094

Cited by 10 publications

(8 citation statements)

References 58 publications

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“…FCA induced AA model is a chronic, systemic, autoimmune inflammation mediated by T cells. It is very similar to human RA in histopathological and laboratory parameters and is ideal models for screening and studying drugs for treating RA ( Chen C.X et al, 2015 ; Qian et al, 2017 ). AA rats mainly manifested as multiple peripheral arthritis and local joint swelling, deformity, pathological changes of proliferative synovitis, articular cartilage damage, bone erosion, inflammatory cell infiltration.…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory Mechanism of Geniposide: Inhibiting the Hyperpermeability of Fibroblast-Like Synoviocytes via the RhoA/p38MAPK/NF-κB/F-Actin Signal Pathway

Deng

et al. 2018

Front. Pharmacol.

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Geniposide (GE) is the extraction and purification of iridoid glycosides from the Gardenia jasminoides Ellis, which is a promising anti-inflammatory drug, but its mechanism of actions on rheumatoid arthritis (RA) has not been clarified. This study investigated the molecular mechanism behind GE reduced the high permeability of fibroblast-like synoviocytes (FLSs) derived from SD rats with adjuvant arthritis (AA), with the aims of observing the action of GE in AA rats and exploring new therapeutic strategies for RA treatment. The CCK-8 method was used to detect FLSs proliferation. The pro-inflammatory cytokines levels and anti-inflammatory cytokines levels in FLSs were determined by ELISA kits. FLSs permeability assay was performed on Transwell. Immunofluorescence was used to assay the arrangement and morphology of F-actin. The expression of the key molecules related to FLSs permeability (RhoA, p-p38MAPK, NF-κB p-p65 and F-actin) was detected by western blotting. After treatment with lipopolysaccharide (LPS), the proliferation and the permeability of the cells increased significantly (all P < 0.05). The expression of RhoA, p-p38MAPK, NF-κB p-p65 and F-actin in FLSs was higher compared with the control group, and F-actin was redistributed, with the formation of additional stress fibers. But, these conditions were moderated after treatment with GE. We demonstrated that the treatment of different concentrations of GE (25, 50, and 100 μg/mL) had a significant inhibitory effect on the proliferation and permeability of FLSs in vitro. Furthermore, the levels of interleukin (IL)-1β and IL-17 secreted by FLSs were decreased in different doses of GE groups, and the levels of anti-inflammatory cytokines (IL-4, TGF-β1) were increased. Under treatment with GE, low expression of RhoA downregulated expression of p-p38MAPK, NF-κB p-p65, and F-actin while compared with control group, and restored the hyperpermeability of FLSs due to LPS treatment. Taken together, GE might play its anti-inflammatory and immunoregulatory effects via regulating the relative equilibrium of pro-inflammatory cytokines and anti-inflammatory cytokines. GE attenuated the hyperpermeability of FLSs. The down-regulation of the conduction of RhoA/p38MAPK/NF-κB/F-actin signal may play a critical role in the mechanisms of GE on RA. GE could be an effective therapeutic agent for the treatment of RA.

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Section: Discussionmentioning

confidence: 99%

Anti-inflammatory Mechanism of Geniposide: Inhibiting the Hyperpermeability of Fibroblast-Like Synoviocytes via the RhoA/p38MAPK/NF-κB/F-Actin Signal Pathway

Deng

et al. 2018

Front. Pharmacol.

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“…In another study, Zhu et al demonstrated that cobrotoxin, a short-chain neurotoxin form NNAV, ameliorated body inflammatory reactions on three rodent experimental inflammation models: formaldehyde-induced mouse foot swelling test, mouse abdominal capillary osmosis test, and Whatman paper-inducing rat granuloma formation test [ 54 ]. Cardiotoxin from NNAV also presented anti-inflammatory actions on formalin test, egg-white-induced non-specific inflammation test, formalin-soaked filter papers triggered granuloma test, and abdominal capillary osmosis test [ 55 ]. These studies illustrated that cobra venom and neurotoxins possessed anti-inflammatory capabilities.…”

Section: Effect Of Nnav and Its Components On Inflammation And Immmentioning

confidence: 99%

“…In the research of NNAV, Zhu [ 11 ] proved that NNAV ameliorated paw edema and pathological lesions in adjuvant arthritis rats, and NNAV also reduced serum TNF-α levels and elevated serum interleukin-10 (IL-10) concentrations, indicating that NNAV may relieve adjuvant arthritis via attenuating inflammation. Furthermore, Chen [ 55 ] demonstrated that cardiotoxin from NNAV administrated to rats obtained a significantly lower mean arthritic score versus model adjuvant arthritis rats in pathological sections. Meanwhile, cardiotoxin decreased serum pro-inflammatory cytokines interleukin-6 (IL-6) and IL-17 expressions, while selectively inhibiting CD4 + T subsets on peripheral blood cells in adjuvant arthritis rats.…”

Section: Research Of Nnav and Its Components On Inflammatory And Imentioning

confidence: 99%

Anti-Inflammatory and Immune Regulatory Actions of Naja naja atra Venom

Wang

Qin

2018

Toxins

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Naja naja atra venom (NNAV) is composed of various proteins, peptides, and enzymes with different biological and pharmacological functions. A number of previous studies have reported that NNAV exerts potent analgesic effects on various animal models of pain. The clinical studies using whole venom or active components have confirmed that NNAV is an effective and safe medicine for treatment of chronic pain. Furthermore, recent studies have demonstrated that NNAV has anti-inflammatory and immune regulatory actions in vitro and in vivo. In this review article, we summarize recent studies of NNAV and its components on inflammation and immunity. The main new findings in NNAV research show that it may enhance innate and humoral immune responses while suppressing T lymphocytes-mediated cellular immunity, thus suggesting that NNAV and its active components may have therapeutic values in the treatment of inflammatory and autoimmune diseases.

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“…Previous research also indicates that LPS could induce the formation of multinucleated cells with expressed TRAP protein via the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs) pathways [ 24 ]. On the other hand, adjuvant-induced arthritis (AIA) and type II collagen-induced arthritis (CIA) are also widely used animal models for the study of RA, and for evaluating the therapeutic potential of anti-RA agents [ 25 , 26 , 27 ]. High levels of pro-inflammatory cytokines and TRAP-positive multinucleated cells that drive RA progression have also been detected in animal models [ 28 , 29 , 30 ].…”

Section: Introductionmentioning

confidence: 99%

Excavatolide B Attenuates Rheumatoid Arthritis through the Inhibition of Osteoclastogenesis

et al. 2017

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Osteoclasts are multinucleated giant cells of macrophage/monocyte lineage, and cell differentiation with the upregulation of osteoclast-related proteins is believed to play a major role in the destruction of the joints in the course of rheumatoid arthritis (RA). Pro-inflammatory cytokines, such as interleukin-17A (IL-17A) and macrophage colony-stimulating factor (M-CSF), can be overexpressed in RA and lead to osteoclastogenesis. In a previous study, we found that cultured-type soft coral-derived excavatolide B (Exc-B) exhibited anti-inflammatory properties. In the present study, we thus aimed to evaluate the anti-arthritic activity of Exc-B in in vitro and in vivo models. The results demonstrated that Exc-B inhibits LPS-induced multinucleated cell and actin ring formation, as well as TRAP, MMP-9, and cathepsin K expression. Additionally, Exc-B significantly attenuated the characteristics of RA in adjuvant (AIA) and type II collagen-induced arthritis (CIA) in rats. Moreover, Exc-B improved histopathological features, and reduced the number of TRAP-positive multinucleated cells in the in vivo AIA and CIA models. Immunohistochemical analysis showed that Exc-B attenuated the protein expression of cathepsin K, MMP-2, MMP-9, CD11b, and NFATc1 in ankle tissues of AIA and CIA rats. Level of interleukin-17A and macrophage colony-stimulating factor were also decreased by Exc-B. These findings strongly suggest that Exc-B could be of potential use as a therapeutic agent by inhibiting osteoclast differentiation in arthritis. Moreover, this study also illustrates the use of the anti-inflammatory marine compound, Exc-B, as a potential therapeutic strategy for RA.

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Suppression of Inflammation and Arthritis by Orally Administrated Cardiotoxin fromNaja naja atra

Cited by 10 publications

References 58 publications

Anti-inflammatory Mechanism of Geniposide: Inhibiting the Hyperpermeability of Fibroblast-Like Synoviocytes via the RhoA/p38MAPK/NF-κB/F-Actin Signal Pathway

Anti-inflammatory Mechanism of Geniposide: Inhibiting the Hyperpermeability of Fibroblast-Like Synoviocytes via the RhoA/p38MAPK/NF-κB/F-Actin Signal Pathway

Anti-Inflammatory and Immune Regulatory Actions of Naja naja atra Venom

Excavatolide B Attenuates Rheumatoid Arthritis through the Inhibition of Osteoclastogenesis

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