Morin exerts antiosteoarthritic properties: an in vitro and in vivo study

2012 ◽  
Vol 237 (4) ◽  
pp. 380-386 ◽  
Author(s):  
Wei-Ping Chen ◽  
Peng-Fei Hu ◽  
Jia-Peng Bao ◽  
Li-Dong Wu
Keyword(s):  
Rat Model ◽  
Cruciate Ligament ◽  
Interleukin 1 ◽  
Cartilage Degradation ◽  
In Vivo Study ◽  
In Vivo Studies ◽  
Tissue Inhibitors Of Metalloproteinase ◽  
Mitogen Activated Protein

Morin is a flavonoid isolated from members of the Moraceae family. Morin has been reported to possess antioxidative and anticarcinogenic activities. However, the antiosteoarthritic properties of morin have not been investigated. In this study, we evaluate the antiarthritic properties of morin through in vitro and in vivo studies. We examined the effects of morin on the expression levels of matrix metalloproteinase (MMP)-3, MMP-13 and tissue inhibitors of metalloproteinase (TIMP)-1 in interleukin-1 β (IL-1 β)-induced rat chondrocytes by realtime polymerase chain reaction and Western blotting. The effects of morin on the phosphorylation of mitogen-activated protein kinases were also investigated. The in vivo antiosteoarthritic effects of morin were evaluated in the rat model of anterior cruciate ligament transection (ACLT)-induced osteoarthritis (OA). We found that morin inhibited the expression of MMP-3 and MMP-13 and increased the expression of TIMP-1 in IL-1 β-induced rat chondrocytes. In addition, morin inhibited IL-1 β-induced phosphorylation of extracellular signal-regulated kinase and p38. For the in vivo study in a rat model of OA induced by ACLT, in which morin was orally administered to rat, the results show that morin suppressed cartilage degradation. Our results suggest that morin may be considered as a possible therapeutic agent for the treatment of OA.

scholarly journals A Novel Synthesized Sulfonamido-Based Gallate-JEZTC Blocks Cartilage Degradation on Rabbit Model of Osteoarthritis: An in Vitro and in Vivo Study

2018 ◽  
Vol 49 (6) ◽  
pp. 2304-2319 ◽  
Author(s):  
Zhenhui Lu ◽  
Qin Liu ◽  
Lei Liu ◽  
Huayu Wu ◽  
Li Zheng ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Cruciate Ligament ◽  
Interleukin 1 ◽  
Rabbit Model ◽  
Cartilage Degradation ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Histological Evaluation ◽  
Chondrocyte Apoptosis

Background/Aims: 3, 4, 5-trihydroxy-N-{4-[(5-methylisoxazol-3-yl) sulfamoyl] phenyl} benzamide (JEZTC), synthesized from gallic acid (GA) and sulfamethoxazole (SMZ), was reported with chondroprotective effects. However, the effects of JEZTC on osteoarthritis (OA) are still unclear. The goal of this study was to investigate the anti-osteoarthritic properties of JEZTC on interleukin-1-beta (IL-1β) stimulated chondrocytes in vitro and a rabbit anterior cruciate ligament transaction (ACLT) OA model in vivo. Methods: Changes in matrix metalloproteinases (MMPs) and apoptosis genes (bax, caspase 3 and tnf-α) and OA-specific protein (MMP-1) expression in vitro and in vivo were detected by real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and immunohistochemistry. The production of reactive oxygen species (ROS) were investigated upon the treatment of JEZTC in chondrocytes processed with IL-1β in vitro and OA in vivo. Effect of JEZTC on OA was further studied by the macroscopic and histological evaluation and scores. The key proteins in signaling pathways inMAPK/P38, PI3KAkt and NF-κB also determined using western blot (WB) analysis. Results: JEZTC could significantly suppress the expression of MMPs and intracellular ROS, while meaningfully increase the gene expression of tissue inhibitor of metalloproteinase-1 (TIMP-1). Moreover, there was less cartilage degradation in JEZTC group compared with the phosphate-buffered saline (PBS) group in vivo. Results also indicated that JEZTC exerts effect on OA by regulating MAPKs and PI3K/Akt signaling pathways to activate NF-κB pathway, leading to the down-regulation of MMPs. The chondro-protective effect of JEZTC may be related with its ability to inhibit chondrocyte apoptosis by reduction of ROS production. Conclusion: JEZTC may be a possible therapeutic agent in the treatment of OA.

scholarly journals Stigmasterol blocks cartilage degradation in rabbit model of osteoarthritis.

2012 ◽  
Vol 59 (4) ◽  
Author(s):  
Wei-Ping Chen ◽  
Chong Yu ◽  
Peng-Fei Hu ◽  
Jia-Peng Bao ◽  
Jing-Li Tang ◽  
...  
Keyword(s):  
Cruciate Ligament ◽  
Rabbit Model ◽  
Cartilage Degradation ◽  
Tissue Inhibitors Of Metalloproteinase ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Group 2 ◽  
Group 1

Stigmasterol has been shown exhibit anti-osteoarthritic properties in vitro studies. However, the in vivo effects of stigmasterol on cartilage are still unclear. This study investigated the anti-osteoarthritic properties of stigmasterol on cartilage degradation in a rabbit model of osteoarthritis (OA). Twenty rabbits underwent bilateral anterior cruciate ligament transection (ACLT) to induce OA. Five rabbits were used as normal control. Two weeks after operation, the rabbits were randomly divided into two groups. Each group of 10 rabbits received intra-articular injection with 0.3 ml of stigmasterol in left knees and vehicle in right knees, once weekly. Group 1 was killed 6 weeks after ACLT and 2 were sacrificed 9 weeks after ACLT. The knee joints were assessed by gross morphology, histology and gene expression analysis. We found that expression of genes encoding matrix metalloproteinases (MMPs) was significantly higher while tissue inhibitors of metalloproteinase (TIMP)-1 was significantly lower in the both joints of the two OA groups compared to normal controls. Stigmasterol reduced the cartilage degradation as assessed by histological analysis and markedly suppressed MMPs expression both in group 1 and group 2. Our results suggest that stigmasterol may be considered as a possible therapeutical agent in the treatment of OA.

scholarly journals Baicalein Inhibits MMPs Expression via a MAPK-Dependent Mechanism in Chondrocytes

2015 ◽  
Vol 36 (1) ◽  
pp. 325-333 ◽  
Author(s):  
Wei-Ping Chen ◽  
Yan Xiong ◽  
Peng-Fei Hu ◽  
Jia-Peng Bao ◽  
Li-Dong Wu
Keyword(s):  
Cruciate Ligament ◽  
Interleukin 1 ◽  
Cartilage Damage ◽  
Rabbit Model ◽  
Mitogen Activated Protein Kinase ◽  
Scutellaria Baicalensis Georgi ◽  
The Matrix ◽  
Mitogen Activated Protein

Background: Baicalein is a flavonoid isolated from Scutellaria baicalensis Georgi. Here, we investigated the anti-osteoarthritic effect of baicalein in vitro and in vivo. Methods: Interleukin-1 beta (IL-1β)-induced chondrocytes were treated with different concentrations of baicalein, real-time PCR and ELISA were performed to detect the matrix metalloproteinases (MMPs) expression. Western blot was used to evaluate the mitogen-activated protein kinase (MAPK) expression. In experimental osteoarthritis (OA), rabbits were treated with baicalein, gross morphological and histological assessment was performed to evaluate the cartilage damage. Results: Baicalein significantly reduced the expression of MMPs in vitro and in vivo. Moreover, baicalein significantly reduced the phosphorylation of p38 and extracellular signal regulated kinase (ERK), but not of c-Jun N-terminal kinase (JNK). In addition, intra-articular injection of baicalein ameliorated the cartilage damage in a rabbit model of OA induced by anterior cruciate ligament transection (ACLT). Conclusions: The results indicate that baicalein may be considered as a potential agent for OA treatment.

scholarly journals Artemisinin Ameliorates Osteoarthritis by Inhibiting the Wnt/β-Catenin Signaling Pathway

2018 ◽  
Vol 51 (6) ◽  
pp. 2575-2590 ◽  
Author(s):  
Gang Zhong ◽  
Ruiming Liang ◽  
Jun Yao ◽  
Jia Li ◽  
Tongmeng Jiang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Cruciate Ligament ◽  
Interleukin 1 ◽  
Cartilage Degradation ◽  
Chondrocyte Apoptosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cell Viability Assay ◽  
Necrosis Factor Alpha ◽  
Anti Inflammatory

Background/Aims: Current drug therapies for osteoarthritis (OA) are not practical because of the cytotoxicity and severe side-effects associated with most of them. Artemisinin (ART), an antimalarial agent, is well known for its safety and selectivity to kill injured cells. Based on its anti-inflammatory activity and role in the inhibition of OA-associated Wnt/β-catenin signaling pathway, which is crucial in the pathogenesis of OA, we hypothesized that ART might have an effect on OA. Methods: The chondro-protective and antiarthritic effects of ART on interleukin-1-beta (IL-1β)-induced and OA patient-derived chondrocytes were investigated in vitro using cell viability assay, glycosaminoglycan secretion, immunofluorescence, quantitative reverse transcription-polymerase chain reaction, and western blotting. We also used OA model rats constructed by anterior cruciate ligament transection and medial meniscus resection (ACLT+MMx) in the joints to investigate the effects of ART on OA by gross observation, morphological staining, immunohistochemistry, and enzyme-linked immunosorbent assay. Results: ART exhibited potent anti-inflammatory effects by inhibiting the expression of proinflammatory chemokines and cytokines, including interleukin (IL)-1β, IL-6, tumor necrosis factor alpha, and matrix metallopeptidase-13. It also showed favorable chondro-protective effect as evidenced by enhanced cell proliferation and viability, increased glycosaminoglycan deposition, prevention of chondrocyte apoptosis, and degeneration of cartilage. Further, ART inhibited OA progression and cartilage degradation via the Wnt/β-catenin signaling pathway, suggesting that it might serve as a Wnt/β-catenin antagonist to reduce inflammation and prevent cartilage degradation. Conclusion: In conclusion, ART alleviates IL-1β-mediated inflammatory response and OA progression by regulating the Wnt/β-catenin signaling pathway. Thereby, it might be developed as a potential therapeutic agent for OA.

In vitro and in vivo studies on the degradation and biosafety of Mg-Zn-Ca-Y alloy hemostatic clip with the carotid artery of SD rat model

2020 ◽  
Vol 115 ◽  
pp. 111093
Author(s):  
Xiao Yu ◽  
Dongyang Li ◽  
Yuanchao Liu ◽  
Pengfei Ding ◽  
Xianghui He ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Rat Model ◽  
In Vivo Studies ◽  
Sd Rat

Gigantol Alleviates IL-1β-Induced Inflammation and Catabolism in Mouse Osteoarthritis via PI3K/Akt/NF-κB Pathways In Vivo and In Vitro

2021 ◽  
Author(s):  
Gaosheng Zhu ◽  
Keze Miao ◽  
Mingwei Dong ◽  
Jie Cai ◽  
Zhihao Shen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Therapeutic Option ◽  
Interleukin 1 ◽  
Cartilage Degradation ◽  
Research Society ◽  
Necrosis Factor Alpha ◽  
Persistent Inflammation ◽  
Anti Inflammatory

Abstract Osteoarthritis (OA), a prevalent disabling disease, is characterized by irreversible cartilage degradation and persistent inflammation. The etiology as well as pathogenesis of OA are not completely unclear and need further investigation. Gigantol, is a bibenzyl derivative extracted from Dendrobium plants and has been found exhibit multiple effects such as anti-inflammatory effects. Nevertheless, the biological function of gigantol on osteoarthritis (OA) is still uncertain. This study aimed at examining the anti-inflammatory effects and latent mechanisms of gigantol in IL-1β-mediated OA progression. In vitro, we identified that gigantol treatment suppressed tumor necrosis factor-alpha (TNF-α), nitric oxide (NO), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS) and interleukin-6 (IL-6) in interleukin-1 beta (IL-1β) mediated mouse OA chondrocytes. Gigantol was also shown to dose dependently downregulate the metalloproteinase 13 (MMP13) as well as thrombospondin motifs 5 (ADAMTS5) levels. Moreover, IL-1β-mediated AKT and PI3K phosphorylation as well as NF-κB activation were inhibited by gigantol. Meanwhile, in vivo, we detected that gigantol treatment inhibited degradation of the cartilage degradation and lowered the Osteoarthritis Research Society International scores (OARSI) in OA mouse. Therefore, gigantol is a promising therapeutic option for OA.

scholarly journals P010 The effect of interleukin-1 receptor antagonism in the management of intestinal inflammation; an in vitro and in vivo study

2013 ◽  
Vol 7 ◽  
pp. S14
Author(s):  
K. Arvanitidis ◽  
E. Filidou ◽  
V. Valatas ◽  
E. Kouroumalis ◽  
V. Paspaliaris ◽  
...  
Keyword(s):  
Intestinal Inflammation ◽  
Interleukin 1 ◽  
In Vivo Study ◽  
Receptor Antagonism

scholarly journals LncRNA CRNED Hinders The Progression of Osteoarthritis By Epigenetic Regulation of DACT1

2021 ◽  
Author(s):  
Ziqi Zhang ◽  
Pei Yang ◽  
Chunsheng Wang ◽  
Run Tian
Keyword(s):  
Rat Model ◽  
Epigenetic Modification ◽  
Colorectal Neoplasia ◽  
Cruciate Ligament ◽  
Cartilage Damage ◽  
Cartilage Degeneration ◽  
Downstream Target ◽  
Age Related

Abstract Osteoarthritis (OA) is mainly characterized by articular cartilage degeneration, synovial fibrosis, and inflammation. LncRNA CRNED (colorectal neoplasia differentially expressed) has been reported to be down-regulated in age-related OA, but its role in injury-induced OA needs to be further explored. In this study, an OA rat model was established by using anterior cruciate ligament transection, and the adenovirus-mediated CRNED overexpression (Ad-CRNED) or DACT1 (dapper antagonist of catenin-1) interference (sh-DACT1) vectors were injected into the rat model via tail vein. Besides, chondrocyte‑like ATDC5 cells were treated with IL-1β (10 ng/mL) to simulate OA conditions in vitro. We found that overexpression of CRNED alleviated cartilage damage and synovitis in OA rats, and suppressed IL-1β-induced apoptosis, inflammation, and extracellular matrix (ECM) degradation in chondrocyte‑like ATDC5 cells, while silencing DACT1 effectively antagonized the protective effect of CRNED both in vivo and in vitro. Mechanism studies revealed that DACT1 could act as a downstream target of CRNED. By recruiting p300, CRNED promoted the enrichment of H3K27ac in the DACT1 promoter, thus promoting DACT1 transcription. In addition, CRNED hindered the activation of the Wnt/β-catenin pathway in IL-1β-stimulated cells by inducing DACT1 expression. In conclusion, CRNED promoted DACT1 expression through epigenetic modification and restrained the activation of Wnt/β-catenin signaling to impede the progression of OA.

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