Resveratrol Protects Murine Chondrogenic ATDC5 Cells Against LPS-Induced Inflammatory Injury Through Up-Regulating MiR-146b

Jin, Hui; Zhang, Hong; Ma, Tingjian; Lan, Hongjia; Shi, Feng; Zhu, Haiyan; Ji, Youbo

doi:10.1159/000490141

Cited by 26 publications

(20 citation statements)

References 20 publications

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“…These data strongly indicate that the intra-articular injection of resveratrol significantly prevents the destruction of OA cartilage tissue through the stimulation of SIRT1, thus reducing the expression of HIF-2α and catabolic elements [138]. Recently, resveratrol has been found to exert anti-inflammatory activity in chondrocytes by upregulating miR-146b, thereby deactivating the NF-κB and p38MAPK signaling pathways [141]. The results of all these studies suggest that resveratrol actually acts as a multitargeting agent by modulating the inflammatory and apoptotic pathway in several steps.…”

Section: Resveratrolmentioning

confidence: 73%

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Herbal Remedies as Potential in Cartilage Tissue Engineering: An Overview of New Therapeutic Approaches and Strategies

et al. 2020

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It is estimated that by 2023, approximately 20% of the population of Western Europe and North America will suffer from a degenerative joint disease commonly known as osteoarthritis (OA). During the development of OA, pro-inflammatory cytokines are one of the major causes that drive the production of inflammatory mediators and thus of matrix-degrading enzymes. OA is a challenging disease for doctors due to the limitation of the joint cartilage’s capacity to repair itself. Though new treatment approaches, in particular with mesenchymal stem cells (MSCs) that integrate the tissue engineering (TE) of cartilage tissue, are promising, they are not only expensive but more often do not lead to the regeneration of joint cartilage. Therefore, there is an increasing need for novel, safe, and more effective alternatives to promote cartilage joint regeneration and TE. Indeed, naturally occurring phytochemical compounds (herbal remedies) have a great anti-inflammatory, anti-oxidant, and anabolic potential, and they have received much attention for the development of new therapeutic strategies for the treatment of inflammatory diseases, including the prevention of age-related OA and cartilage TE. This paper summarizes recent research on herbal remedies and their chondroinductive and chondroprotective effects on cartilage and progenitor cells, and it also emphasizes the possibilities that exist in this research area, especially with regard to the nutritional support of cartilage regeneration and TE, which may not benefit from non-steroidal anti-inflammatory drugs (NSAIDs).

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Section: Resveratrolmentioning

confidence: 73%

“…Jin [141] Mouse chondrogenic cells were treated with 30 µM resveratrol for 24 h and 10 µg/mL LPS for 12 h. Cell viability, apoptosis and the release of pro-inflammatory cytokines was assessed.…”

Section: In Vitro/porcine Chondrocytesmentioning

confidence: 99%

Herbal Remedies as Potential in Cartilage Tissue Engineering: An Overview of New Therapeutic Approaches and Strategies

et al. 2020

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“…Zhang L et al found that miR-146b was down-regulated in chronic nonbacterial prostatitis and might be a effective target for patient treatment (24). Moreover, miR-146b participated in LPS-induced inflammation and apoptosis in murine chondrogenic ATDC5 cells (25). In our study, we displayed that miR-146b up-regulation attenuated pediatric pneumonia progression through facilitating cell viability, suppressing cell apoptosis, decreasing production of IL-6, TNF-α and IL-1β.…”

Section: Discussionmentioning

confidence: 56%

MiR-146b protects against pediatric pneumonia progression through MyD88/NF-κB signaling pathway

Zhang

Dong

Tang

et al. 2019

Preprint

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Background Pneumonia is a common respiratory disease worldwide that can be prevented and treated. However, it is considered to be the leading cause of children death. The present study was aimed to explore the role of miR-146b and its underlying mechanism in lipopolysaccharide (LPS)-induced inflammation injury in pediatric pneumonia. Methods Human fibroblasts WI-38 cells treated with LPS were subjected to construct cell model with inflammation injury. QRT-PCR or Western blot was applied to detect miR-146b and MyD88 expression. ELISA kit was used to analyze the production of pro-inflammatory factors. Cell viability was evaluated by CCK-8 assay. The apoptosis proteins and the downstream genes of NF-κB pathway were detected by Western blot. Results We displayed that miR-146b was downregulated, whereas MyD88 was upregulated in children with pneumonia and in WI-38 cells treated with LPS. Moreover, re-expression of miR-146b suppressed the production of inflammatory factors in the serum of pneumonia patients and WI-38 cells. Also, elevating miR-146b expression increased cell viability and reduced cell apoptosis. However, MyD88 overturned the protective effect of miR-146b on inflammation injury in pediatric pneumonia. Moreover, miR-146b overexpression inhibited the activation of NF-κB signaling pathway by suppressing MyD88. Conclusions These findings revealed that miR-146b attenuated the inflammation injury in pediatric pneumonia through inhibiting MyD88/NF-κB signaling pathway.

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“…Chondrocytes were pre-seeded in 6-well plate and maintained with growth medium for overnight. LPS (Sigma-Aldrich, USA, 20 μg/ml) was added to the medium to induce OA-like inflammation response, as described previously [27]. In order to produce an early stage of inflammation, the chondrocytes were treated with LPS for 3 to 6 h, and produce a late stage of inflammation using a treatment for 24 or 48 h. As to the Glycyrrhizin treatment, its working concentration was 25 μM.…”

Section: Inflammation Of Chondrocytes Induced By Lpsmentioning

confidence: 99%

Dual regulatory roles of HMGB1 in inflammatory reaction of chondrocyte cells and mice

Wenzhao

Song

et al. 2019

Cell Cycle

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Osteoarthritis (OA) is one of the most common bone diseasesas it is reported that the impact of knee osteoarthritis symptomatic form is estimated at 240/100,000 people per year. The inflammation of articular cartilageis thought to be the pathologic drive for development of this disease. HMGB1(high mobility group box-1), a regulatory factor for gene transcription, could stimulate inflammation response. However, theexact regulatory role of HMGB1 in the inflammation of articular cartilage still need to be elucidated. In the current study, we used Quantitative Real-Time PCR(Q-PCR) to detect them RNA levels of Collagen Type II Alpha 1(Col2a1), Aggrecan, MMP3 (Matrix Metallopeptidase 3), MMP13, ADAMTs4 and ADAMTs5; Enzyme-Linked Immunosorbent Assay(ELISA) was used to detect the content of IL-1β and calpain protein; Cell apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay and flow cytometryanalysis; Western blot and immunofluorescence assays were applied to assess the expression of HMGB1; Lastly autophagic activity was mainly verified by monodansylcadaverine (MDC) staining. Our data revealed that in the early stage of chondrocyte inflammation(3 and 6 h of LPS stimulation), cytosolic HMGB1 attenuated inflammation response by facilitating cell autophagy and preventing cell apoptosis. While in the late stage (24 and 48 h of LPS stimulation), the extracellular HMGB1 stimulated inflammation reaction and contributed to the cartilage destruction in OA.

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Resveratrol Protects Murine Chondrogenic ATDC5 Cells Against LPS-Induced Inflammatory Injury Through Up-Regulating MiR-146b

Cited by 26 publications

References 20 publications

Herbal Remedies as Potential in Cartilage Tissue Engineering: An Overview of New Therapeutic Approaches and Strategies

Herbal Remedies as Potential in Cartilage Tissue Engineering: An Overview of New Therapeutic Approaches and Strategies

MiR-146b protects against pediatric pneumonia progression through MyD88/NF-κB signaling pathway

Dual regulatory roles of HMGB1 in inflammatory reaction of chondrocyte cells and mice

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