Abstract
Osteoarthritis (OA) is a degenerative disease of the cartilage that isprevalent in the middle-aged and elderly demography. Polydatin (PD), a naturalresveratrol glucoside, has shown significant anti-inflammatory and anti-arthriticpotential in previous studies. This study was designed to evaluate the therapeuticproperties of PD in vitro and in vivo, and elucidate their underlying mechanisms. Theexpression levels of all relevant factors were evaluated by qRT-PCR, westernblotting, and immunohistochemistry (IHC) where suitable. Reactive oxygen species(ROS) and apoptosis were analyzed using the suitable probes and flow cytometry. Thehistological evidence of cartilage was assessed in rat models, moreover, the severalserum cytokines levels and autophagy levels were evaluated. The result showed PDdisplayed significant chondro-protective effects, inferred in terms of reducedinflammation and cartilage degradation, apoptosis inhibition, and lower ROSproduction. The protective effects were attenuated by the autophagy inhibitor 3-MA,indicating a mediating role of autophagy in PD action. Mechanistically, PD exertedits effects by inhibiting the MAPK and PI3K/Akt signaling pathways which led to thedown-regulation of mTOR. In conclusion, PD protects against cartilage degenerationby activating the autophagy flux in the chondrocytes via the MAPK and PI3K/Aktsignaling pathways.
Highlights
R Osteoarthritis (OA) is a degenerative disease of the cartilage that is prevalent in the middle-aged A and elderly demography
PD protects chondrocytes against IL-1β-induced apoptosis and structural disintegration
The chondrocytes were treated with varying concentrations of PD, and no apparent toxicity was seen for doses between 0.31 to 160 μg/ml (Fig. 1B), toxic was observed at high concentrations (≥320 μg/ml)
Summary
R Osteoarthritis (OA) is a degenerative disease of the cartilage that is prevalent in the middle-aged A and elderly demography. This study was designed to evaluate the therapeutic properties of PD in vitro and in vivo, and elucidate their underlying mechanisms. The expression levels of all relevant factors were evaluated by qRT-PCR, western blotting, and. Reactive oxygen species (ROS) and apoptosis were analyzed using the suitable probes and flow cytometry. The histological evidence of cartilage was assessed in rat models, the several serum cytokines levels and autophagy levels were. The result showed PD displayed significant chondro-protective effects, inferred in terms of reduced inflammation and cartilage degradation, apoptosis inhibition, and lower ROS production. The protective effects were attenuated by the autophagy inhibitor 3-MA, indicating a mediating role. PD exerted its effects by inhibiting the MAPK and PI3K/. C cartilage degeneration by activating the autophagy flux in the chondrocytes via the MAPK and PI3K/
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