Acteoside inhibits inflammatory response via JAK/STAT signaling pathway in osteoarthritic rats

Qiao, Zhiguang; Tang, Jiaxin; Wu, Wen; Tang, Jian; Liu, Ming

doi:10.1186/s12906-019-2673-7

Cited by 43 publications

(31 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Recently, similar with our study, Qiao et al, have reported that acteoside inhibits in ammatory response in OA-induced animals [55]. They showed the suppression of in ammatory cytokines through the inactivation of JAK/STAT signaling pathway in the synovial tissue of DMM-induced OA animals that were administered intraperitoneal injection of acteoside [55]. However, to estimate the effectiveness of acteoside as an OA preventive supplement, acteoside were orally administrated to DMM-induced OA animals in present study.…”

Section: Discussionsupporting

confidence: 92%

“…Therefore, our results consistently indicate that acteoside counteract the IL-1β-induced catabolic effects such as the expression of cartilage degrading enzymes and the production of pro-in ammatory cytokines and in ammatory mediators through the inactivation of cellular signaling pathways such as MAPK and NFκB in the primary rat chondrocytes. Recently, similar with our study, Qiao et al, have reported that acteoside inhibits in ammatory response in OA-induced animals [55]. They showed the suppression of in ammatory cytokines through the inactivation of JAK/STAT signaling pathway in the synovial tissue of DMM-induced OA animals that were administered intraperitoneal injection of acteoside [55].…”

Section: Discussionsupporting

confidence: 88%

See 1 more Smart Citation

Acteoside counteracts interleukin-1β-induced catabolic processes through the modulation of mitogen-activated protein kinases and the NFκB cellular signaling pathway

Lim

Kim

et al. 2020

Preprint

View full text Add to dashboard Cite

Objectives To verify the anti-catabolic effects of acteoside [α-L-rhamnosyl-(1->3)-β-D-glucoside] against osteoarthritis and its anti-catabolic signaling pathway. Methods Primary rat chondrocytes were isolated enzymatically from the articular cartilage of rat knee joint. Cytotoxicity of acteoside was assessed by MTT and Cell Live/Dead assay. Proteoglycan content was measured by dimethylmethylene blue assay. The proteoglycan loss was assessed by histological analysis using safranin-O & fast green staining after ex vivo organ culture of articular cartilage. The alteration of catabolic factors such as cartilage degrading enzymes, pro-inflammation cytokines, and inflammatory mediators were assessed by qPCR, qRT-PCR, gelatin zymography, western blot, and cytokine array. Cellular signaling pathways were investigated by western blot and nucleus translocation. Acteoside was orally administrated to osteoarthritic animals generated by the destabilization of medial meniscus at the knee joint of mice for 8 weeks. Thereafter, proteoglycan loss was assessed by safranin-O & fast green staining. Results Acteoside did not decrease the viabilities of mouse fibroblast L929 cells used as a normal cells and primary rat chondrocytes. Acteoside counteracted the IL-1β-induced proteoglycan loss in the chondrocytes and articular cartilage through suppressing the expression and activation of cartilage-degrading enzyme such as matrix metalloproteinase (MMP)-13, MMP-1, and MMP-3. Furthermore, acteoside suppressed the expression of inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2 in the primary rat chondrocytes treated with IL-1β. Subsequently, the expression of pro-inflammatory cytokines was decreased by acteoside in the primary rat chondrocytes treated with IL-1β. Moreover, acteoside suppressed not only the phosphorylation of mitogen-activated protein kinases in primary rat chondrocytes treated with IL-1β but also the translocation of NFκB from the cytosol to the nucleus through suppression of its phosphorylation. Oral administration of 5 and 10 mg/kg acteoside attenuated the progressive degeneration of articular cartilage in the osteoarthritic mouse model generated by destabilization of the medial meniscus. Conclusion Our findings indicate that acteoside is a promising potential anti-catabolic agent or supplement to attenuate or prevent progressive degeneration of articular cartilage.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 88%

Acteoside counteracts interleukin-1β-induced catabolic processes through the modulation of mitogen-activated protein kinases and the NFκB cellular signaling pathway

Lim

Kim

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…Therefore, our results consistently indicate that acteoside counteract the IL-1 β -induced catabolic effects such as the expression of cartilage-degrading enzymes and the production of proinflammatory cytokines and inflammatory mediators through the inactivation of cellular signaling pathways such as MAPK and NF κ B in the primary rat chondrocytes. Recently, similar with our study, Qiao et al have reported that acteoside inhibits inflammatory response in OA-induced animals [ 55 ]. They showed the suppression of inflammatory cytokines through the inactivation of the JAK/STAT signaling pathway in the synovial tissue of DMM-induced OA animals that were administered intraperitoneal injection of acteoside [ 55 ].…”

Section: Discussionsupporting

confidence: 91%

Acteoside Counteracts Interleukin‐1β‐Induced Catabolic Processes through the Modulation of Mitogen‐Activated Protein Kinases and the NFκB Cellular Signaling Pathway

Lim

Kim

et al. 2021

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Osteoarthritis (OA) is the most common degenerative joint disease with chronic joint pain caused by progressive degeneration of articular cartilage at synovial joints. Acteoside, a caffeoylphenylethanoid glycoside, has various biological activities such as antimicrobial, anti-inflammatory, anticancer, antioxidative, cytoprotective, and neuroprotective effect. Further, oral administration of acteoside at high dosage does not cause genotoxicity. Therefore, the aim of present study is to verify the anticatabolic effects of acteoside against osteoarthritis and its anticatabolic signaling pathway. Acteoside did not decrease the viabilities of mouse fibroblast L929 cells used as normal cells and primary rat chondrocytes. Acteoside counteracted the IL-1β-induced proteoglycan loss in the chondrocytes and articular cartilage through suppressing the expression and activation of cartilage-degrading enzyme such as matrix metalloproteinase- (MMP-) 13, MMP-1, and MMP-3. Furthermore, acteoside suppressed the expression of inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2 in the primary rat chondrocytes treated with IL-1β. Subsequently, the expression of proinflammatory cytokines was decreased by acteoside in the primary rat chondrocytes treated with IL-1β. Moreover, acteoside suppressed not only the phosphorylation of mitogen-activated protein kinases in primary rat chondrocytes treated with IL-1β but also the translocation of NFκB from the cytosol to the nucleus through suppression of its phosphorylation. Oral administration of 5 and 10 mg/kg acteoside attenuated the progressive degeneration of articular cartilage in the osteoarthritic mouse model generated by destabilization of the medial meniscus. Our findings indicate that acteoside is a promising potential anticatabolic agent or supplement to attenuate or prevent progressive degeneration of articular cartilage.

show abstract

“…27 It was suggested that the IL-6 receptor was also an underlying therapeutic target in OA drug development, which could improve degradation of cartilage extracellular protein through the JAK/STAT signal pathways. 28 Previous studies have also reported that FOXM1 knockdown could weaken the inflammatory reaction of cartilage cells in human OA, 13 and FOXM1 expression was increased in cartilage cells treated by IL-1b. FOXM1 knockdown weakened IL-1b-induced cell viability decline, and inhibited the .…”

Section: Discussionmentioning

confidence: 89%

FOXM1 activates JAK1/STAT3 pathway in human osteoarthritis cartilage cell inflammatory reaction

Zeng

Lü

Lin

et al. 2020

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

Osteoarthritis (OA), the most prevalent form of arthritis disease, is characterized by destruction of articular cartilage, osteophyte development, and sclerosis of subchondral bone. Transcription factors Janus kinase 1/signal transducer and activator of transcription 3 (JAK1/STAT3) and Forkhead box M1 (FOXM1) are key mediators of this inflammatory reaction. In this study, we investigated the interaction between JAK1/STAT3 and FOXM1 in OA. Inflammation is related to the cartilage damage, and lipopolysaccharides (LPS) are a major pro-inflammatory inducer, so LPS was utilized to stimulate chondrocytes and establish a cell-based OA model. We found LPS treatment caused a generation of inflammatory cell factors (IL-1β, IL-6, and TNF-α), and upregulation of inducible nitric oxide synthases (iNOS), cyclooxygenase-2 (COX-2), nitric oxide (NO), prostaglandin E2 (PGE2) and other inflammatory mediators. Cell viability of chondrocytes was impaired with LPS stimulation, along with an upregulation of JAK1 expression, and phosphorylation and nuclear accumulation of STAT3. The administration of STAT3 inhibitor WP1066, which abated activation and nuclear location of STAT3, depleted the effect of LPS on inflammation and cell death. Co-immunoprecipitation showed that STAT3 was able to bind to FOXM1, and deactivation of STAT3 resulted in the downregulation of FOXM1. Moreover, FOXM1 silencing inhibited the generation of inflammatory cytokines induced by LPS, and the attenuation of cell survival. These findings indicated that the interaction between JAK1/STAT3 and FOXM1 may play a key role in OA pathogenic studies, and suggest the JAK1/STAT3 pathway may be a potential target for OA therapy.

show abstract

Acteoside inhibits inflammatory response via JAK/STAT signaling pathway in osteoarthritic rats

Cited by 43 publications

References 32 publications

Acteoside counteracts interleukin-1β-induced catabolic processes through the modulation of mitogen-activated protein kinases and the NFκB cellular signaling pathway

Acteoside counteracts interleukin-1β-induced catabolic processes through the modulation of mitogen-activated protein kinases and the NFκB cellular signaling pathway

Acteoside Counteracts Interleukin‐1β‐Induced Catabolic Processes through the Modulation of Mitogen‐Activated Protein Kinases and the NFκB Cellular Signaling Pathway

FOXM1 activates JAK1/STAT3 pathway in human osteoarthritis cartilage cell inflammatory reaction

Contact Info

Product

Resources

About