Effects of Bauhinia championii (Benth.) Benth. polysaccharides on the proliferation and cell cycle of chondrocytes

Cai, Lun; Ye, Hongzhi; Yu, Fangrong; Li, Huiting; Chen, Jiashou; Liu, Xianxiang

doi:10.3892/mmr.2013.1368

Cited by 7 publications

(6 citation statements)

References 27 publications

(24 reference statements)

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“…3, following treatment with 50, 100 and 200 µg/ml of BCBPs, the cell viability increased by 8.96±1.66, 15.75±2.75 and 9.58±1.59, respectively when compared with the untreated group (treated with 0 µg/ml BCBPs) (P<0.01, P<0.05). These results confirmed that treatment with BCBPs promoted chon drocyte proliferation in a time-dependent manner, as shown in our previous study (19).…”

Section: Resultssupporting

confidence: 92%

“…Thus, promoting chondrocyte proliferation may be an efficient method for the treatment of OA. In our previous study, we demonstrated that BCBPs promoted chondrocyte proliferation (19); however, the precise molecular mechanisms responsible for the effects of BCBPs on chondrocyte proliferation have not yet been fully elucidated. In this study, we investigated the mechanisms responsible for the effects of BCBPs on the Wnt/β-catenin signaling pathway in chondrocytes to build a scientific foundation for the use of BCBPs in the treatment of OA.…”

Section: Discussionmentioning

confidence: 97%

“…Previous studies have shown that polysaccharides have vital biological activities in a number of plants, such as inducing immunomodulatory, anti-tumorigenic and wound-healing effects (9), as well as promoting cell proliferation (10)(11)(12)(13). In our previous study, BCB polysaccharides (BCBPs) were shown to induce chondrocyte proliferation by promoting the G1/S transition (19). However, it is yet not clear whether BCBPs promote chondrocyte proliferation by activating the Wnt/β-catenin signaling pathway.…”

Section: Introductionmentioning

confidence: 98%

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Bauhinia championi (Benth.) Benth. polysaccharides upregulate Wnt/β-catenin signaling in chondrocytes

Liu

et al. 2013

International Journal of Molecular Medicine

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Bauhinia championi (Benth.) Benth. polysaccharides (BCBPs), extracted from Bauhinia championi (Benth.) Benth., which has been used in traditional Chinese medicine (TCM) for the treatment of osteoarthritis (OA), are the bioactive constituents of Bauhinia championi (Benth.) rattan. However, the molecular mechanisms responsible for their effects on OA are poorly understood. The Wnt/β-catenin signaling pathway plays an important role in the proliferation of chondrocytes. In the present study, the effects of BCBPs on Wnt/β-catenin signaling in chondrocytes were investigated. BCBPs were obtained by hot-water extraction and identified by the modified high performance liquid chromatography (HPLC) method. Chondrocytes were isolated from the knees of Sprague‑Dawley rats and identified by type II collagen immunohistochemistry. The chondrocytes were treated with or without BCBPs for 48 h. Cell viability was evaluated by MTT assay. The mRNA and protein levels of Wnt-4, β-catenin, Frizzled-2, glycogen synthase kinase (GSK)-3β, cyclin D1 and collagen II were detected by western blot analysis and reverse transcription PCR (RT-PCR), respectively. We found that the BCBPs contained at least seven monosaccharides, including D-mannose, rhamnose, D-(+) glucuronic acid, D-(+) galacturonic acid, D-glucose, galactose and arabinose. The cell viability of the chondrocytes treated with 50, 100 and 200 µg/ml BCBPs was significantly higher than that of the chondroctyes in the control group (treated with 0 µg/ml BCBPs). Furthermore, compared with the control group, the mRNA and protein expression of Wnt-4, β-catenin, Frizzled-2 and cyclin D1 in the BCBP-treated groups markedly increased, whereas the mRNA and protein expression of GSK-3β significantly decreased. Of note, the dose of 100 µg/ml BCBPs was more effective than the dose of 50 µg/ml BCBPs and 200 µg/ml BCBPs. In addition, we found that treatment with BCBPs upregulated the protein levels of collagen II in the chondrocytes. These results indicate that BCBPs upregulate Wnt/β-catenin signaling, thus promoting chondrocyte proliferation.

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Section: Resultssupporting

confidence: 92%

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 98%

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Bauhinia championi (Benth.) Benth. polysaccharides upregulate Wnt/β-catenin signaling in chondrocytes

Liu

et al. 2013

International Journal of Molecular Medicine

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“…The cover slips were rapidly washed in ethanol, dried, and mounted for microscopic examination. The expression of type II collagen was observed using immunohistochemical staining [ 18 ]. Images were captured at a magnification of ×20.…”

Section: Methodsmentioning

confidence: 99%

Millimeter Wave Treatment Inhibits Apoptosis of Chondrocytes via Regulation Dynamic Equilibrium of Intracellular Free Ca²⁺

et al. 2015

Evidence-Based Complementary and Alternative Medicine

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The molecular mechanisms of TNF-α-induced apoptosis of chondrocyte and the role of Ca2+ mediating the effects of MW on TNF-α-induced apoptosis of chondrocytes remained unclear. In this study, we investigated the molecular mechanism underlying inhibiting TNF-α-induced chondrocytes apoptosis of MW. MTT assay, DAPI, and flow cytometry demonstrated that MW significantly increased cell activity and inhibited chromatin condensation accompanying the loss of plasma membrane asymmetry and the collapse of mitochondrial membrane potential. Our results also indicated that MW reduced the elevation of [Ca2+]i in chondrocytes by LSCM. Moreover, MW suppressed the protein levels of calpain, Bax, cytochrome c, and caspase-3, while the expressions of Bcl-2, collagen II, and aggrecan were increased. Our evidences indicated that MW treatment inhibited the apoptosis of chondrocytes through depression of [Ca2+]i. It also inhibited calpain activation, which mediated Bax cleavage and cytochrome c release and initiated the apoptotic execution phase. In addition, MW treatment increased the expression of collagen II and aggrecan of chondrocytes.

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“…The second-generation chondrocytes were fixed with 4% paraformaldehyde in 24-well plates for 30 min, washed three times with PBS, permeabilized for 20 min with 0.5% Triton X-100 in PBS at 4 °C, blocked for 30 min with 3% BSA, and probed overnight at 4 °C with anti-Collagen II (1:100) or LC3(1:100) in 3% BSA. After three rinses with 3% BSA, the cells were probed for 3 h with a secondary antibody (EarthOx, 1:50) in 3% BSA at room temperature, and the nuclei were stained with DAPI for 10 min [ 27 ]. Images were captured using an inverted fluorescence microscope (Nikon).…”

Section: Methodsmentioning

confidence: 99%

Oxymatrine protects articular chondrocytes from IL-1β-induced damage through autophagy activation via AKT/mTOR signaling pathway inhibition

Lu,

Bian,

Wang

et al. 2024

J Orthop Surg Res

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Background Osteoarthritis (OA) is a common degenerative joint disease characterized by persistent articular cartilage degeneration and synovitis. Oxymatrine (OMT) is a quinzolazine alkaloid extracted from the traditional Chinese medicine, matrine, and possesses anti-inflammatory properties that may help regulate the pathogenesis of OA; however, its mechanism has not been elucidated. This study aimed to investigate the effects of OMT on interleukin-1β (IL-1β)-induced damage and the potential mechanisms of action. Methods Chondrocytes were isolated from Sprague-Dawley rats. Toluidine blue and Collagen II immunofluorescence staining were used to determine the purity of the chondrocytes. Thereafter, the chondrocytes were subjected to IL-1β stimulation, both in the presence and absence of OMT, or the autophagy inhibitor 3-methyladenine (3-MA). Cell viability was assessed using the MTT assay and SYTOX Green staining. Additionally, flow cytometry was used to determine cell apoptosis rate and reactive oxygen species (ROS) levels. The protein levels of AKT, mTOR, LC3, P62, matrix metalloproteinase-13, and collagen II were quantitatively analyzed using western blotting. Immunofluorescence was used to assess LC3 expression. Results OMT alleviated IL-1β-induced damage in chondrocytes, by increasing the survival rate, reducing the apoptosis rates of chondrocytes, and preventing the degradation of the cartilage matrix. In addition, OMT decreased the ROS levels and inhibited the AKT/mTOR signaling pathway while promoting autophagy in IL-1β treated chondrocytes. However, the effectiveness of OMT in improving chondrocyte viability under IL-1β treatment was limited when autophagy was inhibited by 3-MA. Conclusions OMT decreases oxidative stress and inhibits the AKT/mTOR signaling pathway to enhance autophagy, thus inhibiting IL-1β-induced damage. Therefore, OMT may be a novel and effective therapeutic agent for the clinical treatment of OA.

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Effects of Bauhinia championii (Benth.) Benth. polysaccharides on the proliferation and cell cycle of chondrocytes

Cited by 7 publications

References 27 publications

Bauhinia championi (Benth.) Benth. polysaccharides upregulate Wnt/β-catenin signaling in chondrocytes

Bauhinia championi (Benth.) Benth. polysaccharides upregulate Wnt/β-catenin signaling in chondrocytes

Millimeter Wave Treatment Inhibits Apoptosis of Chondrocytes via Regulation Dynamic Equilibrium of Intracellular Free Ca²⁺

Oxymatrine protects articular chondrocytes from IL-1β-induced damage through autophagy activation via AKT/mTOR signaling pathway inhibition

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Effects of Bauhinia championii (Benth.) Benth. polysaccharides on the proliferation and cell cycle of chondrocytes

Cited by 7 publications

References 27 publications

Bauhinia championi (Benth.) Benth. polysaccharides upregulate Wnt/β-catenin signaling in chondrocytes

Bauhinia championi (Benth.) Benth. polysaccharides upregulate Wnt/β-catenin signaling in chondrocytes

Millimeter Wave Treatment Inhibits Apoptosis of Chondrocytes via Regulation Dynamic Equilibrium of Intracellular Free Ca2+

Oxymatrine protects articular chondrocytes from IL-1β-induced damage through autophagy activation via AKT/mTOR signaling pathway inhibition

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Millimeter Wave Treatment Inhibits Apoptosis of Chondrocytes via Regulation Dynamic Equilibrium of Intracellular Free Ca²⁺