Stachydrine attenuates IL-1β-induced inflammatory response in osteoarthritis chondrocytes through the NF-κB signaling pathway

Wu, Hao; Zhang, Minghui; Li, Weihua; Zhu, Shutao; Zhang, Dengfeng

doi:10.1016/j.cbi.2020.109136

Cited by 26 publications

(16 citation statements)

References 26 publications

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“…Eight weeks after the administration of puerarin, the surface roughness of the tibia and femoral cartilage was weakened, the chondrocytes were arranged more neatly, and the number of inflammatory cells was greatly reduced. Increases in cytokines such as IL‐1β, IL‐6, TNF‐α in cartilage tissue are the main feature of OA, and inflammation plays a central role in the development of OA (Ansari, Ahmad, & Haqqi, 2020; H. Wu, Zhang, Li, Zhu, & Zhang, 2020). In the early stages of OA, catabolic activity is increased, which is associated with the increased expression of inflammatory mediators, cartilage‐degrading proteinases, and stress response factors.…”

Section: Discussionmentioning

confidence: 99%

Puerarin inhibits the development of osteoarthritis through antiinflammatory and antimatrix‐degrading pathways in osteoarthritis‐induced rat model

Wen

Song

et al. 2020

Phytotherapy Research

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Puerarin is an isoflavone isolated from the medicinal plant Pueraria lobata. The purpose of this study was to study the antiinflammatory and antimatrix-degrading effects of puerarin in a rat osteoarthritis (OA) model and its protective effects on joints. The rat OA model was established by anterior cruciate ligament transection (ACLT) surgery. Rats (n = 40) were divided into nontreated OA, OA + celecoxib (2.86 mg/kg), OA + puerarin (50 and 100 mg/kg), and control groups.Two weeks after surgical induction, puerarin was administered by gavage daily for 8 weeks. After 8 weeks, macroscopic observation and histopathological images showed that cartilage damage was reduced after puerarin and celecoxib treatment, the intensity of Safranin O staining was high, and the OARSI scores were significantly reduced compared to the OA group. Puerarin reduced the expression of MMP-3, MMP-13, ADAMTS-5, and COX-2 in the cartilage tissue of ACLT rats, inhibited the production of IL-1β, IL-6, and TNF-α inflammatory factors, increased Type II collagen content, and altered the expression of serum OA cartilage degradation/bone turnover biomarkers (CTX-I, CTX-II, COMP, and PIINP). Based on these findings, we speculate that puerarin supplement to attain recovery from OA damage.

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Section: Discussionmentioning

confidence: 99%

Puerarin inhibits the development of osteoarthritis through antiinflammatory and antimatrix‐degrading pathways in osteoarthritis‐induced rat model

Wen

Song

et al. 2020

Phytotherapy Research

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“…Chondrocytes (5 × 10 5 /well) were obtained at passage 2 and cultured in ProNectin F-coated Bioflex six-well culture plates (Flexcell International) to 80% confluence (Liu et al 2017 ). The chondrocytes were treated with 10 ng/ml of interleukin (IL)-1β in the culture medium for 12 h as per a previous study (Wu et al 2020 ). Untreated chondrocytes were used as controls.…”

Section: Methodsmentioning

confidence: 99%

CircHYBID regulates hyaluronan metabolism in chondrocytes via hsa-miR-29b-3p/TGF-β1 axis

Liao

Zhang

Chen

et al. 2021

Mol Med

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Background Hyaluronan (HA) metabolism by chondrocytes is important for cartilage development and homeostasis. However, information about the function of circular RNAs (circRNAs) in HA metabolism is limited. We therefore profiled the role of the novel HA-related circRNA circHYBID in the progression of osteoarthritis (OA). Methods CircHYBID function in HA metabolism in chondrocytes was investigated using gain-of-function experiments, and circHYBID mechanism was confirmed via bioinformatics analysis and luciferase assays. The expression of circHYBID–hsa-miR-29b-3p–transforming growth factor (TGF)-β1 axis was examined by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. CircHYBID, TGF-β1, and HA levels in cartilage samples were evaluated using qRT-PCR and pathological examination. Enzyme-linked immunosorbent assay was used to assess HA accumulation in chondrocyte supernatant. Results CircHYBID expression was significantly downregulated in damaged cartilage samples compared with that in the corresponding intact cartilage samples. CircHYBID expression was positively correlated with alcian blue score. Interleukin-1β stimulation in chondrocytes downregulated circHYBID expression and decreased HA accumulation. Gain-of-function experiments revealed that circHYBID overexpression in chondrocytes increased HA accumulation by regulating HA synthase 2 and HYBID expression. Further mechanism analysis showed that circHYBID upregulated TGF-β1 expression by sponging hsa-miR-29b-3p. Conclusions Our results describe a novel HA-related circRNA that could promote HA synthesis and accumulation. The circHYBID–hsa-miR-29b-3p–TGF-β1 axis may play a powerful regulatory role in HA metabolism and OA progression. Thus, these findings will provide new perspectives for studies on OA pathogenesis, and circHYBID may serve as a potential target for OA therapy.

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“…Numerous studies have revealed that IL-1β can activate the nuclear factor-κB (NF-κB) pathway (14)(15)(16). NF-κB has been identified as an inducible transcription factor (17) and the NF-κB pathway has been reported to regulate the balance in the catabolism that controls numerous inflammation-related genes (18).…”

Section: Changes Of Type II Collagenase Biomarkers On Il-1β-induced Rat Articular Chondrocytesmentioning

confidence: 99%

Changes of type II collagenase biomarkers on IL‑1β‑induced rat articular chondrocytes

Zhang

Shen

et al. 2021

Exp Ther Med

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Osteoarthritis (OA) is characterized by progressive degeneration of cartilage, formation of cartilage at the cartilage edge, and remodeling of the subchondral bone. Pro-inflammatory cytokines [e.g., interleukin (IL)-1β] that induce inflammation and promote chondrocyte damage induce OA. Currently, the diagnosis of OA is commonly based on imaging examinations (e.g., X-ray) and evaluations of clinical symptoms; however, biomarkers that can effectively diagnose OA are currently not available. By studying the mechanism underlying OA cartilage injury and changes in the concentrations of the biomarkers procollagen type II carboxy-terminal propeptide (PIICP), collagen type-II C-telopeptide fragments (CTX-II), and type II collagen cleavage neoepitope (C2C) during pathogenesis, the present study established a theoretical basis for the evaluation and early diagnosis of OA. In an experiment, 10 ng/ml IL-1β was used to the treat chondrocyte-induced OA models in vitro for 0, 12, 24 and 48 h. Western blotting was used to detect the expression levels of matrix metalloproteinase (MMP)-3, MMP-13, and inducible nitric oxide synthase (iNOS) protein at each time-point. The concentrations of CTX-II, C2C, and PIICP in the cell culture supernatant were detected by ELISA kit. A biochemical kit was used to detect changes of nitric oxide (NO) in the cell culture supernatant. In addition, chondrocytes were treated with 10 ng/ml IL-1β for 0, 30, 60 and 90 min and the translocation and phosphorylation of the NF-κB pathway were investigated by western blotting. Following IL-1β stimulation, the NF-κB pathway was activated to increase the expression levels of MMPs and iNOS synthesis downstream of the pathway, resulting in an increased degradation of type II collagen (Col II). To sum up, pro-inflammatory IL-1β induced an OA chondrocyte model. During the development of OA, the expression of MMPs and NO increased and Col II was degraded.

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Stachydrine attenuates IL-1β-induced inflammatory response in osteoarthritis chondrocytes through the NF-κB signaling pathway

Cited by 26 publications

References 26 publications

Puerarin inhibits the development of osteoarthritis through antiinflammatory and antimatrix‐degrading pathways in osteoarthritis‐induced rat model

Puerarin inhibits the development of osteoarthritis through antiinflammatory and antimatrix‐degrading pathways in osteoarthritis‐induced rat model

CircHYBID regulates hyaluronan metabolism in chondrocytes via hsa-miR-29b-3p/TGF-β1 axis

Changes of type II collagenase biomarkers on IL‑1β‑induced rat articular chondrocytes

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