Inhibition effect of <i>Caragana sinica root</i> extracts on Osteoarthritis through MAPKs, NF-κB signaling pathway

Min, Ga-Yul; Park, Jong-Min; Joo, InHwan; Kim, Dong‐Hee

doi:10.7150/ijms.52330

Cited by 12 publications

(10 citation statements)

References 55 publications

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“…Phosphorylated MAPKs (p-ERK1/2, p-JNK, and p-p38) relate MMPs expression and cartilage degradation [50]. The NF-κB pathway is modulated by the MAPKs phosphorylation and is included in the regulation of inflammatory mediators as well as OA progression [51,52]. Normally, NF-κB is localized to the cytoplasm with its inhibitor subunit IκB-α, but IL-1β induced phosphorylation and degradation of IκB, and results in the translocation of NF-κB p65 subunit into the nucleus, resulting in the induction of inflammatory mediators [51,53,54].…”

Section: Discussionmentioning

confidence: 99%

“…The NF-κB pathway is modulated by the MAPKs phosphorylation and is included in the regulation of inflammatory mediators as well as OA progression [51,52]. Normally, NF-κB is localized to the cytoplasm with its inhibitor subunit IκB-α, but IL-1β induced phosphorylation and degradation of IκB, and results in the translocation of NF-κB p65 subunit into the nucleus, resulting in the induction of inflammatory mediators [51,53,54]. Therefore, repression of these pathways is crucial in suppressing inflammation, and several studies have reported that certain plants and naturally derived compounds, such as Caragana sinica root extract, Punica granatum extract, oleuropein, and CQAF, show antiarthritic activity by regulating the MAPK and NF-κB pathways [34,51,52,55].…”

Section: Discussionmentioning

confidence: 99%

“…Normally, NF-κB is localized to the cytoplasm with its inhibitor subunit IκB-α, but IL-1β induced phosphorylation and degradation of IκB, and results in the translocation of NF-κB p65 subunit into the nucleus, resulting in the induction of inflammatory mediators [51,53,54]. Therefore, repression of these pathways is crucial in suppressing inflammation, and several studies have reported that certain plants and naturally derived compounds, such as Caragana sinica root extract, Punica granatum extract, oleuropein, and CQAF, show antiarthritic activity by regulating the MAPK and NF-κB pathways [34,51,52,55]. In this study, 4,5-diCQA treatment inhibited the IL-1β-induced phosphorylation of MAPKs (ERK1/2, JNK, and p38), the degradation of IκB-α, and the translocation of the NF-κB p65 subunit.…”

Section: Discussionmentioning

confidence: 99%

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Chondroprotective Effects of 4,5-Dicaffeoylquinic Acid in Osteoarthritis through NF-κB Signaling Inhibition

et al. 2022

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Osteoarthritis (OA) is characterized by cartilage degradation, inflammation, and pain. The dicaffeoylquinic acid (diCQA) isomer, 4,5-diCQA, exhibits antioxidant activity and various other health-promoting benefits, but its chondroprotective effects have yet to be elucidated. In this study, we aimed to investigate the chondroprotective effects of 4,5-diCQA on OA both in vitro and in vivo. Primary rat chondrocytes were pre-treated with 4,5-diCQA for 1 h before stimulation with interleukin (IL)-1β (5 ng/mL). The accumulation of nitrite, PGE2, and aggrecan was observed using the Griess reagent and ELISA. The protein levels of iNOS, COX-2, MMP-3, MMP-13, ADMATS-4, MAPKs, and the NF-κB p65 subunit were measured by Western blotting. In vivo, the effects of 4,5-diCQA were evaluated for 2 weeks in a destabilization of the medial meniscus (DMM)-surgery-induced OA rat model. 4,5-diCQA significantly inhibited IL-1β-induced expression of nitrite, iNOS, PGE2, COX-2, MMP-3, MMP-13, and ADAMTS-4. 4,5-diCQA also decreased the IL-1β-induced degradation of aggrecan. It also suppressed the IL-1β-induced phosphorylation of MAPKs and translocation of the NF-κB p65 subunit to the nucleus. These findings indicate that 4,5-diCQA inhibits DMM-surgery-induced cartilage destruction and proteoglycan loss in vivo. 4,5-diCQA may be a potential therapeutic agent for the alleviation of OA progression. In this study, diclofenac was set to be administered once every two days, but it showed an effect on OA. These results may be used as basic data to suggest a new dosing method for diclofenac.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Chondroprotective Effects of 4,5-Dicaffeoylquinic Acid in Osteoarthritis through NF-κB Signaling Inhibition

et al. 2022

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“…To further investigate the role of miR-10a-3p in the progression of OA, we first transfected miR-10a-3p mimic into LPS-stimulated chondrocytes. The inflammatory responses are established to promote chondrocyte ECM degradation ( Min et al, 2021 ), therefore, we first detected levels of representative inflammatory factors, IL-1β and TNF-α, in supernatant of chondrocytes by ELISA. The results showed that miR-10a-3p mimic suppressed the enlarged concentration of IL-1β and TNF-α induced by LPS stimulation ( Figure 5A ).…”

Section: Resultsmentioning

confidence: 99%

MicroRNA-10a-3p Improves Cartilage Degeneration by Regulating CH25H-CYP7B1-RORα Mediated Cholesterol Metabolism in Knee Osteoarthritis Rats

Zhang

Shi

et al. 2021

Front. Pharmacol.

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Osteoarthritis (OA) is a worldwide degenerative joint disease that seriously impaired the quality of life of patients. OA has been established as a disease with metabolic disorder. Cholesterol 25-hydroxylase (CH25H) was proved to play a key role in cartilage cholesterol metabolism. However, the biological function and mechanism of CH25H in OA remains further investigation. Growing researches have proved the vital roles of miRNAs in OA progression. In this study, we screened out miR-10a-3p through high-throughput miRNA sequencing which may bind to CH25H. Molecular mechanism investigation indicated that miR-10a-3p is an upstream target of CH25H. Functional exploration revealed miR-10a-3p suppressed the inflammatory responses, cholesterol metabolism and extracellular matrix (ECM) degradation in primary chondrocytes. Moreover, rescue assays implied that miR-10a-3p reversed CH25H plasmids induced inflammatory cytokine production and ECM degradation. Furthermore, the OA rat model was established to explore the function of miR-10a-3p in vivo. The results showed that miR-10a-3p can recover the OA features through targeting CH25H/CYP7B1/RORα axis. In conclusion, these findings implied a crucial role of miR-10a-3p/CH25H/CYP7B1/RORα axis in OA, which may provide a promising therapeutic strategy for OA.

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“…In addition, the OA cartilage also expresses a wide range of NF‐κB‐mediated catabolic chemokines and cytokines, including interleukin (IL)‐6, IL‐8, tumor necrosis factor α (TNFα), IL‐1, and receptor activator of NF‐κB (RANK) ligand MMP synthesis, reduces proteoglycan and collagen synthesis, and operates in a positive feedback loop to improve NF‐κB initiation (Mendonça et al, 2020). Lastly, the NF‐κB molecules increase articular damage by inducing prostaglandin E2 (PGE2), nitric oxide synthase (NOS), cyclooxygenases 2(COX2), and nitric oxide (NO), which promotes the production of cartilage inflammation, catabolic factors, and osteoarthritis chondrocyte cell death (Min et al, 2021).…”

Section: Role Of Nf‐κb In Osteoarthritismentioning

confidence: 99%

Potential role of nutraceuticals via targeting a Wnt/β‐catenin and NF‐κB pathway in treatment of osteoarthritis

Alharbi

Afzal

Altamimi

et al. 2022

Journal of Food Biochemistry

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Osteoarthritis (OA) is a disease due to the aging of the articular cartilage, a post‐mitotic tissue that stays functioning until primary homeostatic processes fail. Because of pain and disability, OA significantly influences national healthcare expenses and patient quality of life. It is a whole‐joint illness characterized by inflammatory and oxidative signaling pathways and significant epigenetic alterations that cause cartilage extracellular matrix degradation. The canonical Wnt pathway (Wnt/β‐catenin pathway) and nuclear factor kappa B (NF‐κB) signaling pathways may function in joint tissues by modulating the activity of synovial cells, osteoblasts, and chondrocytes. However, finding innovative ways to treat osteoarthritis and get the joint back to average balance is still a struggle. Nutraceuticals are dietary supplements that promote joint health by balancing anabolic and catabolic signals. New therapeutic methods for OA treatment have been developed based on many research findings that show nutraceuticals have strong anti‐inflammation, antioxidant, anti–bone resorption, and anabolic properties. For the treatment of osteoarthritis, we explore the possible involvement of nutraceuticals that target the Wnt/β‐catenin and NF‐κB pathways. Practical applications In keeping with the aging population, osteoarthritis is becoming more widespread. In this extensive research, we studied the role of the Wnt/β‐catenin and NF‐κB pathway in OA formation and progression. Nutraceuticals that target these OA‐related signaling pathways are a viable therapy option. Wnt/β‐catenin and NF‐κB signaling pathway are inhibited by polyphenols, flavonoids, alkaloids, and vitamins from the nutraceutical category, making them possible therapeutic drugs for OA therapy.

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Inhibition effect of Caragana sinica root extracts on Osteoarthritis through MAPKs, NF-κB signaling pathway

Cited by 12 publications

References 55 publications

Chondroprotective Effects of 4,5-Dicaffeoylquinic Acid in Osteoarthritis through NF-κB Signaling Inhibition

Chondroprotective Effects of 4,5-Dicaffeoylquinic Acid in Osteoarthritis through NF-κB Signaling Inhibition

MicroRNA-10a-3p Improves Cartilage Degeneration by Regulating CH25H-CYP7B1-RORα Mediated Cholesterol Metabolism in Knee Osteoarthritis Rats

Potential role of nutraceuticals via targeting a Wnt/β‐catenin and NF‐κB pathway in treatment of osteoarthritis

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