Exercise and Osteoarthritis

Chen, Lei; Yu, Yan

doi:10.1007/978-981-15-1792-1_15

Cited by 21 publications

(17 citation statements)

References 97 publications

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“…Osteoarthritis (OA) is a common joint disease with destruction of articular cartilages [ 1 ]. OA has seriously affected the life quality of human beings, and there is no effective strategy for treatment of OA [ 2 ]. Chondrocyte dysfunction is the leading cause of cartilage degeneration and OA progression [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Circ_0005526 contributes to interleukin-1β-induced chondrocyte injury in osteoarthritis via upregulating transcription factor 4 by interacting with miR-142-5p

Wahafu

Tuo

et al. 2022

Bioengineered

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Circular RNAs (circRNAs) can regulate the progression of osteoarthritis (OA) via serving as competing endogenous RNAs (ceRNAs). This work was performed for functional research of circ_0005526 in Interleukin-1β (IL-1β)-induced OA injury. Circ_0005526, microRNA-142-5p (miR-142-5p) or transcription factor 4 (TCF4) expression was measured via reverse transcription-quantitative polymerase chain reaction assay. Cell analysis was performed by Cell Counting Kit-8 assay for cell viability, EdU assay for cell proliferation and flow cytometry for cell apoptosis. The protein level detection was conducted using western blot. Target analysis was carried out via dual-luciferase reporter assay and RNA pull-down assay. Circ_0005526 was upregulated in OA cartilage tissues and IL-1β-exposed chondrocyte cells. IL-1β inhibited cell viability and proliferation but enhanced cell apoptosis and inflammation, then these damages were attenuated after downregulation of circ_0005526. Circ_0005526 interacted with miR-142-5p, and circ_0005526 knockdown suppressed IL-1β-induced OA progression through upregulating miR-142-5p. TCF4 was regulated by circ_0005526 via targeting miR-142-5p. The function of circ_0005526 was also achieved by upregulation of TCF4. These results unraveled that circ_0005526 promoted IL-1β-induced chondrocyte injury in OA via suppressing miR-142-5p binding to TCF4.

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Section: Introductionmentioning

confidence: 99%

Circ_0005526 contributes to interleukin-1β-induced chondrocyte injury in osteoarthritis via upregulating transcription factor 4 by interacting with miR-142-5p

Wahafu

Tuo

et al. 2022

Bioengineered

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“…It is characterized by progressive degeneration, joint hyperplasia, joint space narrowing, and extracellular matrix (ECM) metabolism and is the most prevalent and disabling form of arthritis worldwide 2,3 . The etiology of OA is mainly related to age, strain, obesity, trauma, joint deformities, and congenital abnormalities of joints 4 . Progression of OA is also governed by a multifactorial pathway that is not yet fully elucidated and understood.…”

Section: Introductionmentioning

confidence: 99%

“…2,3 The etiology of OA is mainly related to age, strain, obesity, trauma, joint deformities, and congenital abnormalities of joints. 4 Progression of OA is also governed by a multifactorial pathway that is not yet fully elucidated and understood. Reduced chondrocyte activity and accelerated development of OA are reportedly due to autophagy and mitochondrial dysfunction.…”

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confidence: 99%

circRNA‐MSR regulates the expression of FBXO21 to inhibit chondrocyte autophagy by targeting miR‐761 in osteoarthritis

Jia

Liu

Wang

2022

The Kaohsiung J of Med Scie

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Osteoarthritis (OA) is a chronic degenerative joint disease and is the most prevalent and disabling form of arthritis worldwide. Autophagy plays a vital role in OA. This study aimed to explore whether covalently closed circular RNA MSR (circRNA-MSR) could affect the Fbox Only Protein 21 (FBXO21) expression by targeting microRNA-761 (miR-761), thereby affecting the autophagy in OA chondrocytes. Clinical OA tissues were collected, and circRNA-MSR, miR-761, and FBXO21 expressions were detected via quantitative real-time polymerase chain reaction (qRT-PCR). An in vitro OA model was constructed by treating C28/I2 cells with LPS and treating them with overexpression or knockdown vector of circRNA-MSR, miR-761, and FBXO21, and autophagy inhibitor 3-MA. Fluorescence in situ hybridization (FISH) determined the location of circRNA-MSR and miR-761. Dual-luciferase assay assessed circRNA-MSR and miR-761, along with the bindings of miR-761 and FBXO21. Cell viability was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. LC3 II/I, p62 and beclin 1 expressions were detected via the western blot. circRNA-MSR and FBXO21 levels were elevated in OA, but miR-761 level was inhibited. Suppressing circRNA-MSR promoted the autophagy of LPS-treated cells. circRNA-MSR could bind to miR-761 and inhibit its expression. MiR-761 inhibition reversed the promoted autophagy caused by circRNA-MSR knockdown in LPS-treated C28/I2 cells. Moreover, miR-761 could target FBXO21 and inhibit its expression. FBXO21 overexpression reversed the increased autophagy caused by miR-761 overexpression in LPS-treated C28/I2 cells. circRNA-MSR could affect FBXO21 level via targeting miR-761, thereby repressing autophagy in OA chondrocytes, providing a new target and strategy for OA treatment.

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“…It is clinically characterized by destruction of articular cartilage, pain, and stiffness, which ultimately lead to immobility and the reduced quality of life for patients, thereby increasing the social and medical burden [ 2 ]. Artificial joint replacement is mainly suitable for advanced patients with severe symptoms, but there is still a lack of substantial progress in the treatment of early and midstage patients [ 3 ]. In-depth study of the pathogenesis of osteoarthritis has important clinical significance for improving the level of diagnosis and treatment of osteoarthritis.…”

Section: Introductionmentioning

confidence: 99%

Study on the Protective Effect and Mechanism of the Rhizoma Drynariae‐Epimedium Formula on Osteoarthritis in Rats

Dai

2022

Contrast Media & Molecular Imaging

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Purpose. The aim of the study was to study the protective effect of the Rhizoma Drynariae-Epimedium formula on osteoarthritis in rats and to explore its mechanism. Methods. Fifty SD rats were randomly divided into 5 groups, namely, the control group, model group, Rhizoma Drynariae group, Epimedium group, and Rhizoma Drynariae-Epimedium group, with 10 rats in each group. Knee arthritis models were established by injecting papain solution (10% papain + 0.03 mol/L L-cysteine mixture) into the knee joint cavity of SD rats on the 0th, 3rd, and 6th days of the experiment, respectively. The model group, Rhizoma Drynariae group, Epimedium group, and Rhizoma Drynariae-Epimedium group were given modeling treatment, while the control group was not given modeling treatment. The Rhizoma Drynariae group, Epimedium group, and the Rhizoma Drynariae-Epimedium group were, respectively, given corresponding solvent gavage treatment. Both the model group and the control group were given an equal volume of normal saline. Once a day, a total of 4 w were administered. The general conditions of the rats were observed and recorded, and the knee joint width and the knee joint swelling degree of the affected side were measured and compared. HE staining and Safranin O-fast green staining were used to compare the structural changes of cartilage. The concentrations of inflammatory factors IL-1β, IL-6, and TNF-α in the joint cavity lavage fluid were determined by using ELISA. The expression of key proteins of the MAPK signaling pathway (p38, p-p38, ERK, p-ERK, JNK, and p-JNK) in joint synovial tissue was determined by western blotting. Results. After modeling, except for the normal activities of the SD rats in the control group, the rest of the groups showed lack of energy and a slight limp in the knee joints. The SD rats in the model group, Rhizoma Drynariae group, Epimedium group, and Rhizoma Drynariae-Epimedium group had local swelling of the knee joint, and the knee joint width was greater than those in the control group ( p < 0.05 ). Compared with the model group, the knee joint swelling of SD rats in the Rhizoma Drynariae group, the Epimedium group, and the Rhizoma Drynariae-Epimedium group was significantly reduced. The knee joint swelling degree of SD rats in the Rhizoma Drynariae-Epimedium group was significantly lower than that in the Rhizoma Drynariae and Epimedium groups. HE staining and Safranin O-fast green staining showed that the cartilage structure of SD rats was severely damaged and eroded, and the subchondral bone mass was reduced. Compared with the model group, the damage of cartilage tissue in the Rhizoma Drynariae group, Epimedium group, and Rhizoma Drynariae-Epimedium group was less severe. In the Rhizoma Drynariae-Epimedium group, cartilage tissue structure damage and erosion were lighter than those of the Rhizoma Drynariae group and the Epimedium group. The concentrations of inflammatory factors IL-1β, IL-6, and TNF-α in the articular cavity lavage fluid of SD rats in the model group, Rhizoma Drynariae group, Epimedium group, and Rhizoma Drynariae-Epimedium group were higher than those in the control group. Compared with the model group, the concentrations of IL-1β, IL-6, and TNF-α in the joint cavity lavage fluid of the Rhizoma Drynariae group, Epimedium group, and Rhizoma Drynariae-Epimedium group were significantly decreased. In the Rhizoma Drynariae-Epimedium group, IL-1β, IL-6, and TNF-α concentrations were lower than those of the Rhizoma Drynariae and Epimedium groups. Compared with the control group, the expression levels of p-p38, p-ERK, and p-JNK proteins in the model group, Rhizoma Drynariae group, Epimedium group, and Rhizoma Drynariae-Epimedium group were significantly increased. The expression levels of p-ERK, p-p38 and p-JNK in the Drynariae group, Epimedium group, and Drynariae-Epimedium group were significantly lower than those in the model group. The expression levels of p-ERK, p-p38, and p-JNK in the Rhizoma Drynariae-Epimedium group were significantly lower than those in the Rhizoma Drynariae and Epimedium groups. Conclusion. The Rhizoma Drynariae-Epimedium formula can play a protective role in the process of osteoarthritis by inhibiting the phosphorylation levels of p38, ERK, and JNK-related proteins in the cartilage tissue MAPK signaling pathway, reducing the inflammatory response.

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Exercise and Osteoarthritis

Cited by 21 publications

References 97 publications

Circ_0005526 contributes to interleukin-1β-induced chondrocyte injury in osteoarthritis via upregulating transcription factor 4 by interacting with miR-142-5p

Circ_0005526 contributes to interleukin-1β-induced chondrocyte injury in osteoarthritis via upregulating transcription factor 4 by interacting with miR-142-5p

circRNA‐MSR regulates the expression of FBXO21 to inhibit chondrocyte autophagy by targeting miR‐761 in osteoarthritis

Study on the Protective Effect and Mechanism of the Rhizoma Drynariae‐Epimedium Formula on Osteoarthritis in Rats

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