Effects of Gentiopicroside on activation of NLRP3 inflammasome in acute gouty arthritis mice induced by MSU

He, Menglin; Hu, Cheng; Chen, Meijuan; Gao, Qian; Li, Liqiu; Tian, Weiqian

doi:10.1007/s11418-021-01571-5

Cited by 19 publications

(9 citation statements)

References 40 publications

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“…Although NSAIDs are commonly used to treat OA, they only provide temporary relief from clinical symptoms and can cause significant side effects in the cardiovascular system, cerebrovascular system, and gastrointestinal tract [ 32 ]. Recently, there has been extensive interest in the use of GPS for the treatment of bone and joint diseases due to its potent anti-inflammatory and analgesic properties [ 19 , 33 , 34 ]. Our study revealed that the use of GPS effectively inhibited the inflammatory response in chondrocytes induced by LPS and alleviated hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

Gentiopicroside ameliorates the lipopolysaccharide-induced inflammatory response and hypertrophy in chondrocytes

Li,

Fan,

Zhao

et al. 2024

J Orthop Surg Res

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Purpose This study aimed to evaluate the protective effects of gentiopicroside against lipopolysaccharide-induced chondrocyte inflammation. Methods SW 1353 chondrosarcoma cells were stimulated with LPS (5 μg/ml) for 24 h and treated with different concentrations of gentiopicroside (GPS) for 24 h. The toxic effects of GPS on chondrocytes were determined using a CCK-8 assay and EdU staining. Western blotting, qPCR, and immunofluorescence analysis were used to examine the protective effect of GPS against the inflammatory response in chondrocytes induced by lipopolysaccharide (LPS). One-way ANOVA was used to compare the differences between the groups (significance level of 0.05). Results The CCK-8 results showed that 10, 20 and 40 μM GPS had no significant toxic effects on chondrocytes; GPS effectively reduced the production of IL-1β and PGE2, reversed LPS-induced extracellular matrix degradation in cartilage by inhibiting the Stat3/Runx2 signaling pathway, and suppressed the hypertrophic transformation of SW 1353 chondrosarcoma cells. Conclusion Our study demonstrated that GPS significantly inhibited the LPS-induced inflammatory response and hypertrophic cellular degeneration in SW 1353 chondrosarcoma cells and is a valuable traditional Chinese medicine for the treatment of knee osteoarthritis.

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Section: Discussionmentioning

confidence: 99%

Gentiopicroside ameliorates the lipopolysaccharide-induced inflammatory response and hypertrophy in chondrocytes

Li,

Fan,

Zhao

et al. 2024

J Orthop Surg Res

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“…Moreover, GPS could suppress pro-infammatory cytokines release, neutrophil infiltration and NLRP3 inflammasome activation. Therefore, the effect of GPS on GA might be ascribed to the inhibition on NLRP3 infammasome ( 80 ). In another original study, the cell viability of THP-1 cells stimulated by LPS and MSU was observed to be significantly improved by epicatechin (EC) in a dose-dependent manner.…”

Section: Therapeutic Strategies For Targeting Nlrp3 In Gamentioning

confidence: 99%

Role of NLRP3 in the pathogenesis and treatment of gout arthritis

Liu

Wang

2023

Front. Immunol.

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Gout arthritis (GA) is a common and curable type of inflammatory arthritis that has been attributed to a combination of genetic, environmental and metabolic factors. Chronic deposition of monosodium urate (MSU) crystals in articular and periarticular spaces as well as subsequent activation of innate immune system in the condition of persistent hyperuricemia are the core mechanisms of GA. As is well known, drugs for GA therapy primarily consists of rapidly acting anti-inflammatory agents and life-long uric acid lowering agents, and their therapeutic outcomes are far from satisfactory. Although MSU crystals in articular cartilage detected by arthrosonography or in synovial fluid found by polarization microscopy are conclusive proofs for GA, the exact molecular mechanism of NLRP3 inflammasome activation in the course of GA still remains mysterious, severely restricting the early diagnosis and therapy of GA. On the one hand, the activation of Nod-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome requires nuclear factor kappa B (NF-κB)-dependent transcriptional enhancement of NLRP3, precursor (pro)-caspase-1 and pro-IL-1β, as well as the assembly of NLRP3 inflammasome complex and sustained release of inflammatory mediators and cytokines such as IL-1β, IL-18 and caspase-1. On the other hand, NLRP3 inflammasome activated by MSU crystals is particularly relevant to the initiation and progression of GA, and thus may represent a prospective diagnostic biomarker and therapeutic target. As a result, pharmacological inhibition of the assembly and activation of NLRP3 inflammasome may also be a promising avenue for GA therapy. Herein, we first introduced the functional role of NLRP3 inflammasome activation and relevant biological mechanisms in GA based on currently available evidence. Then, we systematically reviewed therapeutic strategies for targeting NLRP3 by potentially effective agents such as natural products, novel compounds and noncoding RNAs (ncRNAs) in the treatment of MSU-induced GA mouse models. In conclusion, our present review may have significant implications for the pathogenesis, diagnosis and therapy of GA.

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“…GPS can inhibit the activation of NLRP3 inflammasomes in macrophages under in vitro conditions. GPS can be used to treat gouty arthritis by hindering the activation of the NLRP3 inflammasome [116].…”

Section: Glycosidesmentioning

confidence: 99%

Effects and Mechanisms of Traditional Chinese Medicine and Related Active Constituents Treating Gout

2023

Curr Res Cmpl Alt Med

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Gout is an inherited metabolic disorder resulting from abnormalities in purine metabolism manifesting as episodes of acute inflammatory arthritis. The incidence of gout shows an increasing tendency each year, due to the complicated pathogenesis, the currently available drugs have poor treatment effects on it. Therefore, the development of effective drugs for gout treatment is urgently needed. Because of its high biological activity and safety, Traditional Chinese medicine (TCM) has significant advantages in the prevention and treatment of gout. This paper systematically reviewed the related research on TCM's treatment of gout in the previous five years, and summarized the actions and mechanisms of 25 Chinese herbal extracts, 38 Chinese medicinal monomers, and 19 Chinese medicinal compounds in the treatment of gout, including serum uric acid levels reduction, anti-inflammation, and anti-oxidative stress. These primarily involve the signaling pathways NLRP3/ASC/caspase, TLRs/MYD88/NF-κB, ATP/ P2X7R, and others. Furthermore, the limitations and shortcomings of the experimental study on the treatment of gout with TCM are discussed and appropriate measures are proposed. To summarize, TCM is likely to be a potential candidate for gout treatment, but more clinical research is needed to fully understand its role in the treatment of gout.

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Effects of Gentiopicroside on activation of NLRP3 inflammasome in acute gouty arthritis mice induced by MSU

Cited by 19 publications

References 40 publications

Gentiopicroside ameliorates the lipopolysaccharide-induced inflammatory response and hypertrophy in chondrocytes

Gentiopicroside ameliorates the lipopolysaccharide-induced inflammatory response and hypertrophy in chondrocytes

Role of NLRP3 in the pathogenesis and treatment of gout arthritis

Effects and Mechanisms of Traditional Chinese Medicine and Related Active Constituents Treating Gout

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