Duhuo Jisheng Decoction-containing serum promotes proliferation of interleukin-1β-induced chondrocytes through the p16-cyclin D1/CDK4-Rb pathway

Wu, Guangwen; Fan, Huailing; Huang, Yuanpeng Janet; Zheng, Chengchao; Ye, Jinxia; Liu, Xianxiang

doi:10.3892/mmr.2014.2527

Cited by 13 publications

(14 citation statements)

References 40 publications

(42 reference statements)

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“…We firstly reported that Cyclin D1 was relatively different expressed in different OA grade patients. Wu et al [19] identified that when over-expression of Cyclin D1, the proliferation of chondrocyte was increased. Beier et al [20] further verified the Cyclin D1 in vivo for the promotion of the proliferation of chondrocyte.…”

Section: Discussionmentioning

confidence: 99%

Cyclin D1 regulates osteoarthritis chondrocyte apoptosis via WNT3/β-catenin signalling

Chen

You

Wang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Objective: Cyclin D1 was an important molecular involved in the pathological process of osteoarthritis (OA). The purpose of this study was to identify the effect and potential mechanism of Cyclin D1 for the proliferation and apoptosis of OA chondrocytes. Methods: We used polymerase chain reaction (PCR) method to identify the expression levels of Cyclin D1 and downstream Wnt/b-catenin pathway-related genes in OA chondrocytes according to the grade of OA. Small interfering RNA (siRNA) or overexpression of Cyclin D1 were used to identify the role of Cyclin D1 in cell proliferation and apoptosis. Next, we used XAV-939 to inhibit the Wnt/b-catenin pathway and explore the relevant mechanism. Results: Cyclin D1 was significantly decreased with OA grade (p < .05). After siCyclin D1 transfection, the expression level of WNT3 and nuclear b-catenin were significantly increased, while Wnt10a and total b-catenin were not obviously changed. Co-cultured with XAV-939 and siCyclin D1 abolished the effects of siCyclin D1 on proliferation and apoptosis of OA chondrocytes (p < .05). Conclusions: Cyclin D1 regulated chondrocyte proliferation and apoptosis through Wnt3/b-catenin instead of Wnt10a/b-catenin signalling pathway.

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Section: Discussionmentioning

confidence: 99%

Cyclin D1 regulates osteoarthritis chondrocyte apoptosis via WNT3/β-catenin signalling

Chen

You

Wang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…As shown in Figure 7, DHJSD has an overall effect to eliminate "fenghan-shi", respectively, and thus to relieve pain of "Bi Zheng" through promoting "Gan" and "Shen" function and therefore strengthen the bones and tendons [30] . It also improves circulation and remove stasis of "Qi" and "Xue", reduces tissue swelling and relieves pain [20,22,23,26,32,39,40] . Some pharmacological studies have demonstrated that DHJSD may have effects of analgesia, immune function regulation, blood vessel dilation, anti-inflammation, and antiplatelet aggregation [20,22,23,26,32,39,40] .…”

Section: Discussionmentioning

confidence: 99%

“…It also improves circulation and remove stasis of "Qi" and "Xue", reduces tissue swelling and relieves pain [20,22,23,26,32,39,40] . Some pharmacological studies have demonstrated that DHJSD may have effects of analgesia, immune function regulation, blood vessel dilation, anti-inflammation, and antiplatelet aggregation [20,22,23,26,32,39,40] . In a study of the aging-related osteoarthritis, another common bone degenerative disease, Chen et al found that DHJSD may inhibit VEGF and HIF-1α to retard cartilage degradation in a rabbit model of osteoarthritis [53] .…”

Section: Discussionmentioning

confidence: 99%

“…DHJSD was specifically developed to orchestrate the therapeutic actions to target at the primary (Jun) and secondary (Chen and Zuo) causatives [31] and has an overall effect to eliminate "feng-han-shi" and thus relieves pain of "Bi Zheng" through promoting "Gan" and "Shen" function and reinforcing the bones and tendons [30]. It also improves circulation and removes stasis of "Qi" and "Xue", reduces tissue swelling, and relieves pain [20,22,23,26,32,39,40]. Duhuo (contains osthole) and jisheng target the major etiological problems as "Jun" (or chief) components by eliminating "feng-han-shi" [21].…”

Section: Discussionmentioning

confidence: 99%

“…The main function of SDF-1 is to guide cell migration and to further stimulate the chemotaxis of inflammatory cells and induce cell surface to produce integrins. Our previous studies have shown that the SDF-1 expression and apoptosis in degeneration of human (Poria Cocos), Chuanxiong (Rhizoma Chuanxiong), Danggui (Radix Angelicae Sinensis), Niuxi (Radix Achyranthis Bidentatae), Dihuang (Radix Rehmanniae Preparata), Baishao (Radix Paeoniae Alba), Duzhong (Cortex Eucommiae Ulmoidis), Renshen (Panax ginseng) and Gancao (Radix Glycyrrhizae) [20,22,23,26,39,40] , were mixed and soaked in distilled water, rotary evaporator for rotary steam and the solution was filtered and concentrated [41] . After boiled for 30 min twice the DHJSD solution was filtered (filter 0.22 µm) and then dissolved in DMEM/F12 medium containing 15% fetal bovine serum at a final concentration of 10 mg/mL.…”

Section: Introductionmentioning

confidence: 99%

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Duhuo Jisheng Decoction inhibits SDF-1-induced inflammation and matrix degradation in human degenerative nucleus pulposus cells in vitro through the CXCR4/NF-κB pathway

et al. 2018

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Lower back pain (LBP) is the most common disease in orthopedic clinics world-wide. A classic Fangji of traditional Chinese medicine, Duhuo Jisheng Decoction (DHJSD), has been proven clinically effective for LBP but its therapeutic mechanisms remain unclear. We hypothesized that DHJSD might relieve LBP through inhibiting the exaggerated proinflammatory cytokines and extracellular matrix (ECM) degradation. Thus, we studied the effects of DHJSD on stromal cell-derived factor-1 (SDF-1)-induced inflammation and ECM degradation in human nucleus pulposus cells (hNPCs). The primary hNPCs were isolated from either degenerated human intervertebral disc (HID) of LBP patients or normal HID of lumbar vertebral fracture patients, and cultured in vitro. The cells were treated with SDF-1 (10 ng/mL) and subsequently with different concentrations (100-500 μg/mL) of DHJSD for 24 h, respectively. We found that application of DHJSD significantly antagonized the SDF-1-induced production of proinflammatory cytokines and reduction of aggrecan and type II collagen in the hNPCs. DHJSD also markedly reduced the SDF-1-induced increase of CXCR4 and p-p65 and inhibited the nuclear translocation of p65 in the hNPCs. DHJSD, CXCR4-siRNA, and NF-κB inhibitor (BAY11-7082) caused the same inhibition of exaggerated proinflammatory cytokines in the SDF-1-treated hNPCs. These results provided compelling evidence that DHJSD may inhibit the generation of proinflammatory mediators and ECM degradation of HID through an orchestrated targeting at multiple molecules in the SDF-1/CXCR4/NF-κB pathway, thus offered novel mechanistic insights into the clinical effectiveness of DHJSD on LBP.

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Retracted: Cyclin D1 Gene Silencing Promotes IL‐1β‐Induced Apoptosis in Rat Chondrocytes

Zan

Yao

et al. 2017

J of Cellular Biochemistry

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This study investigated the effects of cyclin D1 gene silencing on cell proliferation and apoptosis of interleukin-1b (IL-1b)-induced osteoarthritis (OA) chondrocytes. Chondrocytes from healthy sprague-dawley rats were divided into blank, OA model (chondrocytes underwent IL-1b inducement), OA trial (chondrocytes underwent IL-1b inducement with cyclin D1-shRNA treatment), and negative control (NC; chondrocytes underwent IL-1b inducement and control-shRNA treatment) groups. Cell proliferation was assessed by CCK-8 assay, and cell cycle and apoptosis by flow cytometry. qRT-PCR and Western blotting were performed to detect cyclin D1 and apoptosisrelated factors expression levels. Chondrocyte proliferation increased after 72-96 h after incubation. The OA trial group exhibited reduced cell proliferation at 48, 72, and 96 h after treatment. The OA model, OA trial, and NC groups all contained more cells arrested in G1 phase and had higher apoptosis rates than the blank group. Additionally, the OA trial group contained more cells arrested in G1 phase, with increased apoptosis rates compared to the OA model and NC groups. The OA model group had lowest expression of cyclin D1 whereas the blank group contained the highest among the four groups. qRT-PCR also showed that the OA model, OA trial, and NC groups all had increased expression levels of Bax and reduced expression levels of Bcl-2 and P53 compared to the blank group, whereby by the OA group had the most significant change. The combined evidence in our study shows that cyclin D1 gene silencing suppresses proliferation and induces apoptosis of rat chondrocytes in IL-1b-induced OA.

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Duhuo Jisheng Decoction-containing serum promotes proliferation of interleukin-1β-induced chondrocytes through the p16-cyclin D1/CDK4-Rb pathway

Cited by 13 publications

References 40 publications

Cyclin D1 regulates osteoarthritis chondrocyte apoptosis via WNT3/β-catenin signalling

Cyclin D1 regulates osteoarthritis chondrocyte apoptosis via WNT3/β-catenin signalling

Duhuo Jisheng Decoction inhibits SDF-1-induced inflammation and matrix degradation in human degenerative nucleus pulposus cells in vitro through the CXCR4/NF-κB pathway

Retracted: Cyclin D1 Gene Silencing Promotes IL‐1β‐Induced Apoptosis in Rat Chondrocytes

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