Protective effects of dioscin against cartilage destruction in a monosodium iodoacetate (MIA)-indcued osteoarthritis rat model

Lu, Jiawei; Zhang, Tingwei; Sun, Huijun; Wang, Sailun; Liu, Mozhen

doi:10.1016/j.biopha.2018.09.075

Cited by 37 publications

(24 citation statements)

References 67 publications

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“…Some natural compounds, such as dioscin (a saponin), and mangiferine (a xanthone glucoside), have up-regulated another isoform, PPARγ in osteoarthritic cartilage and chondrocytes. Dioscin protects the cartilage by antioxidant, anti-apoptotic, and anti-inflammatory effects that down-regulate the canonical Wnt pathway, while mangiferine inhibits IL-1β-induced PGE2 release, canonical NFκB signaling, and activation of MMP-1, and MMP-3 [114,115]. In summary, PPAR molecules are protective for osteoblasts and interfere with multiple cellular pathways, implicating both members of the Wnt family and OPG.…”

Section: Metabolic Regulator Pparβ/δ Is a Putative Link Between Omentioning

confidence: 99%

Regulatory Effects and Interactions of the Wnt and OPG-RANKL-RANK Signaling at the Bone-Cartilage Interface in Osteoarthritis

Kovács

Vajda

Nagy

2019

IJMS

152

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Cartilage and the bordering subchondral bone form a functionally active regulatory interface with a prominent role in osteoarthritis pathways. The Wnt and the OPG-RANKL-RANK signaling systems, as key mediators, interact in subchondral bone remodeling. Osteoarthritic osteoblasts polarize into two distinct phenotypes: a low secretory and an activated, pro-inflammatory and anti-resorptive subclass producing high quantities of IL-6, PGE2, and osteoprotegerin, but low levels of RANKL, thus acting as putative effectors of subchondral bone sclerosis. Wnt agonists, Wnt5a, Wisp-1 initiate excessive bone remodeling, while Wnt3a and 5a simultaneously cause loss of proteoglycans and phenotype shift in chondrocytes, with decreased expression of COL2A, aggrecan, and Sox-9. Sclerostin, a Wnt antagonist possesses a protective effect for the cartilage, while DKK-1 inhibits VEGF, suspending neoangiogenesis in the subchondral bone. Experimental conditions mimicking abnormal mechanical load, the pro-inflammatory milieu, but also a decreased OPG/RANKL ratio in the cartilage, trigger chondrocyte apoptosis and loss of the matrix via degradative matrix metalloproteinases, like MMP-13 or MMP-9. Hypoxia, an important cofactor exerts a dual role, promoting matrix synthesis via HIF-1α, a Wnt silencer, but turning on HIF-2α that enhances VEGF and MMP-13, along with aberrant collagen expression and extracellular matrix deterioration in the presence of pro-inflammatory cytokines.

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Section: Metabolic Regulator Pparβ/δ Is a Putative Link Between Omentioning

confidence: 99%

Regulatory Effects and Interactions of the Wnt and OPG-RANKL-RANK Signaling at the Bone-Cartilage Interface in Osteoarthritis

Kovács

Vajda

Nagy

2019

IJMS

152

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“…Osteoarthritis, emanating from damage to cartilage and underlying bones, can cause pain, stiffness, and deformity and affect millions of people all around the world [156, 157]. In monosodium iodoacetate induced osteoarthritis, the degradation of ECM by MMP13, CHOP-mediated apoptosis of chondrocytes, inflammation, ER stress and oxidative stress could be inhibited by dioscin.…”

Section: Antiarthriticmentioning

confidence: 99%

“…In monosodium iodoacetate induced osteoarthritis, the degradation of ECM by MMP13, CHOP-mediated apoptosis of chondrocytes, inflammation, ER stress and oxidative stress could be inhibited by dioscin. Wnt/ β -catenin signaling, which activates catabolism in chondrocytes, could also be downregulated by dioscin, while PPAR γ , whose activation can lower the production of catabolic factors and ameliorate the oxidative stress, could be upregulated, thus contributing to the protecting effects of dioscin against osteoarthritis [156].…”

Section: Antiarthriticmentioning

confidence: 99%

Recent Advances in the Pharmacological Activities of Dioscin

Yang

Ren

et al. 2019

BioMed Research International

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Dioscin is a typical saponin with multiple pharmacological activities. The past few years have seen an emerging interest in and growing research on this pleiotropic saponin. Here, we review the emerging pharmacological activities reported recently, with foci on its antitumor, antimicrobial, anti-inflammatory, antioxidative, and tissue-protective properties. The potential use of dioscin in therapies of diverse clinical disorders is also discussed.

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“…Modern pharmacological studies have suggested that dioscin exerts anti-inflammatory effects via alleviating the lipopolysaccharide-induced inflammatory kidney injury ( 11 ). Previous studies have revealed that dioscin not only has significant effects on the anti-inflammatory responses, but also exhibits antiviral ( 12 ), antioxidative ( 13 ), hepatoprotective ( 14 ) and antiapoptotic activities ( 15 ). Furthermore, numerous studies have focused on the neuroprotective effects of dioscin following peripheral and central nerve injury ( 16-19 ).…”

Section: Introductionmentioning

confidence: 99%

HMGB‑1/RAGE signaling inhibition by dioscin attenuates hippocampal neuron damage induced by oxygen‑glucose deprivation/reperfusion

et al. 2020

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Cerebral ischemia is one of the most common clinical diseases characterized by high morbidity and mortality. Neurocyte apoptosis and a cascade of inflammatory signals following cerebral ischemia-reperfusion injury (IRI) may contribute to secondary brain damage, resulting in severe neurological damage. It has been reported that dioscin, a natural steroid saponin, exerts anti-inflammatory properties against different diseases. The present study aimed to investigate the role of dioscin in oxygen-glucose deprivation/reperfusion (OGD/R) induction in hippocampal cells in vitro and in vivo . For the in vitro study, hippocampal cells were collected from rat embryos of gestational age of E18. The oxygen-glucose deprivation model in primary hippocampal neurons was used to mimic cerebral IRI in vitro . To select the optimum dioscin concentration and acting time, cell viability was evaluated by a Cell Counting Kit-8 (CCK-8) assay. Neurons subjected to OGD/R were treated with dioscin and the inflammatory cytokines, high mobility group box chromosomal protein 1 (HMGB-1)/receptor for advanced glycation end products (RAGE) signaling molecules and apoptosis-associated genes were determined. The intracellular reactive oxygen species (ROS) generation was detected. Furthermore, the effects of dioscin on the antioxidant defense mechanisms were evaluated by measuring the activity of glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT) and the glutathione (GSH)/glutathione disulphide (GSSG) ratio. In addition, OGD/R-induced cells were transfected with pcDNA3.1-HMGB-1 and treated with dioscin, and the neuronal cell apoptosis rate was determined using a terminal deoxynucleotidyl transferase-mediated 2-deoxyuridine 5-triphosphate-biotin nick-end labeling (TUNEL) assay. The mRNA and protein expression levels of the inflammatory factors were measured using real-time quantitative polymerase chain reaction (RT-qPCR) and western blot analysis, respectively. For the in vivo investigation, the oxidation and anti-oxidation system in rat hippocampal tissue was evaluated by detecting the expression of the aforementioned oxidative stress-associated proteins, 3-NT as well as 8-oxo-deoxyguanosine (8-OHdG). In the hippocampal region, the apoptotic rate was determined using a TUNEL assay. The results demonstrated that dioscin at a dose of 400 ng/ml significantly reversed the increase in the expression levels of the inflammatory factors and attenuated those of apoptotic cytokines induced by OGD/R. Additionally, dioscin notably reversed the OGD/R-mediated activation of the HMGB-1/RAGE signaling pathway in vitro and in vivo . Cell treatment with dioscin significantly attenuated ROS production and increased the activity of antioxidant enzymes. Additionally, increasing the expression of HMGB-1 inhibited the protective effects of dioscin on cell apoptosis in the OGD/R-induced...

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Protective effects of dioscin against cartilage destruction in a monosodium iodoacetate (MIA)-indcued osteoarthritis rat model

Cited by 37 publications

References 67 publications

Regulatory Effects and Interactions of the Wnt and OPG-RANKL-RANK Signaling at the Bone-Cartilage Interface in Osteoarthritis

Regulatory Effects and Interactions of the Wnt and OPG-RANKL-RANK Signaling at the Bone-Cartilage Interface in Osteoarthritis

Recent Advances in the Pharmacological Activities of Dioscin

HMGB‑1/RAGE signaling inhibition by dioscin attenuates hippocampal neuron damage induced by oxygen‑glucose deprivation/reperfusion

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