Jiawei Yanghe decoction ameliorates cartilage degradation in vitro and vivo via Wnt/β-catenin signaling pathway

Xia, Hanting; Cao, Duanguang; Yang, Fo; Yang, Wenlong; Li, Wei; Liu, Pu; Wang, Shuhao; Yang, Fusheng

doi:10.1016/j.biopha.2019.109708

Cited by 29 publications

(21 citation statements)

References 44 publications

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“…Besides its therapeutic effectiveness, it was also characterized by fewer adverse effects. Some studies have demonstrated that parts of TCM ( Liu et al, 2014 ; Wang et al, 2018 ; Xia et al, 2020 ), such as Duo Huo JI Sheng Decoction (DHJSD), Bushen Huoxue Decoction (BSHXD), and Jiawei Yanghe Decoction (JWYHD), could ameliorate OA progression and protect articular chondrocytes. Furthermore, the possible mechanisms of these TCM were analyzed.…”

Section: Discussionmentioning

confidence: 99%

Osteoking Decelerates Cartilage Degeneration in DMM-Induced Osteoarthritic Mice Model Through TGF-β/smad-dependent Manner

Ling

Zeng

et al. 2021

Front. Pharmacol.

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Osteoarthritis (OA) is a common disease characterized by cartilage degeneration. In recent years much attention has been paid to Traditional Chinese Medicine (TCM) since its treatments have shown efficacy for ameliorating cartilage degradation with mild side effects. Osteoking is a TCM prescription that has long been used in OA treatment. However, the exact mechanism of Osteoking are not fully elucidated. In the current study, destabilization of the medial meniscus (DMM)-induced OA mice was introduced as a wild type animal model. After 8 weeks of administration of Osteoking, histomorphometry, OARSI scoring, gait analysis, micro-CT, and immunohistochemical staining for Col2, MMP-13, TGFβRII and pSmad-2 were conducted to evaluate the chondroprotective effects of Osteoking in vivo. Further in vitro experiments were then performed to detect the effect of Osteoking on chondrocytes. TGFβRIICol2ER transgenic mice were constructed and introduced in the current study to validate whether Osteoking exerts its anti-OA effects via the TGF-β signaling pathway. Results demonstrated that in wild type DMM mice, Osteoking ameliorated OA-phenotype including cartilage degradation, subchondral bone sclerosis, and gait abnormality. Col2, TGFβRII, and pSmad-2 expressions were also found to be up-regulated after Osteoking treatment, while MMP-13 was down-regulated. In vitro, the mRNA expression of MMP-13 and ADAMTS5 decreased and the mRNA expression of Aggrecan, COL2, and TGFβRII were up-regulated after the treatment of Osteoking in IL-1β treated chondrocytes. The additional treatment of SB505124 counteracted the positive impact of Osteoking on primary chondrocytes. In TGFβRIICol2ER mice, spontaneous OA-liked phenotype was observed and treatment of Osteoking failed to reverse the OA spontaneous progression. In conclusion, Osteoking ameliorates OA progression by decelerating cartilage degradation and alleviating subchondral bone sclerosis partly via the TGF-β signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Osteoking Decelerates Cartilage Degeneration in DMM-Induced Osteoarthritic Mice Model Through TGF-β/smad-dependent Manner

Ling

Zeng

et al. 2021

Front. Pharmacol.

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“…The present study investigated whether the Wnt/β-catenin pathway, especially β-catenin, was involved in the anti-inflammatory effect of SrR. The Wnt/β-catenin pathway serves a crucial role in chondrocyte proliferation, differentiation and apoptosis ( 37 ) and aggravates OA by promoting MMPs ( 38 ). Wnt/β-catenin signaling in human chondrocytes has an unexpected anticatabolic role by counteracting NF-κB-mediated MMP expression induced by IL-1β in a negative feedback loop ( 39 ).…”

Section: Discussionmentioning

confidence: 99%

The anti‑inflammation effect of strontium ranelate on rat chondrocytes with or without IL‑1β in vitro

Liu

Yang

et al. 2022

Exp Ther Med

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Temporomandibular joint osteoarthritis (TMJ-OA) is a common disease with a high level of inflammation in the joint micro-environment and cartilage degradation. Anti-inflammation and cartilage regeneration are the key therapies for TMJ-OA, but currently, there are no novel medicines or treatments that can control its pathogenic progression. Strontium ranelate (SrR) is an anti-osteoporosis drug and is now considered a promising anti-OA drug, but the anti-inflammatory effect of SrR remains to be elucidated. In the present study, the anti-inflammatory effect of SrR in a normal or high IL-1β environment was observed. Cell viability under the treatment of SrR was tested using Cell Counting Kit-8. Toluidine blue staining, immunofluorescence staining, hydroxyproline assay, PCR assay and western blotting were used to detect the expression of collagen (Col)II, proteoglycans (PG) and aggrecan as a reflection of extracellular matrix synthesis and MMP-9,13 hydroxyproline was used as an inflammation indicator. IL-1β of 10 ng/ml was added to the culture medium as inflammation environment and the tests of those biomarkers were done again. Then, the changes in β-catenin were also studied by immunofluorescence staining, PCR assay and western blotting to explore the possible involvement of the Wnt/β-catenin pathway. The results showed a significant inhibition of MMP-9, MMP-13, β-catenin and promotion of Col-II, PG and aggrecan in normal chondrocytes. The presence of IL-1β markedly upregulated the expression of MMP-9, MMP-13 and β-catenin while suppressing Col-II and PG and SrR partially reversed this trend. In conclusion, SrR decreased MMPs but promoted Col-II, aggrecan and PG synthesis in rat chondrocytes with or without the presence of IL-1β and SrR attenuated the IL-1β-induced increase in β-catenin, thus reducing the inflammatory reaction.

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“…Moreover, there are no effective therapeutic options that can prevent disease progression ( 5 , 6 ). OA is associated with degradation of matrix cartilage and chondrocytes, which are the only type of cell in articular cartilage ( 7 ). Extracellular matrix (ECM) molecules are involved in maintaining the structure and function of regular cartilage, whose components include proteoglycans and collagen, produced by chondrocytes ( 8 ).…”

Section: Introductionmentioning

confidence: 99%

Sulforaphane protects against oxidative stress‑induced apoptosis via activating SIRT1 in mouse osteoarthritis

Chen

Huang

et al. 2021

Mol Med Rep

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osteoarthritis (oa), the most common form of human joint disease, is characterized by progressive degeneration of the articular cartilage, synovitis and subchondral osteoporosis. chondrocyte apoptosis is the primary pathogenic mechanism of oa and is considered to be a potential therapeutic target. Sulforaphane (SFn), a dietary isothiocyanate obtained from cruciferous vegetables, has been reported to exert an anti-apoptotic effect by activating sirtuin 1 (SirT1). To the best of our knowledge, however, the effects of SFn on apoptotic responses in oa have not been reported. in the present study, SFN was shown to significantly inhibit chondrocyte apoptosis while enhancing expression levels of SirT1 in a H 2 o 2 -induced oa mouse model. The anti-apoptotic effect of SFn was reversed by SirT1 small interfering rna, implying that SirT1 exerted a protective role against the effect of SFn on chondrocytes. The expression levels of c/eBP homologous protein, 78-kda glucose regulated protein, Bax, Bcl-2 and cleaved caspase 3 were found to be downregulated in SFn-treated mice. Furthermore, SFn ameliorated cartilage degradation in the OA mouse model. These findings indicate that SFn exerted an anti-apoptotic effect on chondrocytes and ameliorated oa in vivo by activating the SirT1 signaling pathway.

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Jiawei Yanghe decoction ameliorates cartilage degradation in vitro and vivo via Wnt/β-catenin signaling pathway

Cited by 29 publications

References 44 publications

Osteoking Decelerates Cartilage Degeneration in DMM-Induced Osteoarthritic Mice Model Through TGF-β/smad-dependent Manner

Osteoking Decelerates Cartilage Degeneration in DMM-Induced Osteoarthritic Mice Model Through TGF-β/smad-dependent Manner

The anti‑inflammation effect of strontium ranelate on rat chondrocytes with or without IL‑1β in vitro

Sulforaphane protects against oxidative stress‑induced apoptosis via activating SIRT1 in mouse osteoarthritis

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