Immunopharmacology and immunotoxicology · 2022
Echinacoside alleviates osteoarthritis in rats by activating the Nrf2-HO-1 signaling pathway.
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Tan Zhijun, Zhang Bin
Аннотация
OBJECTIVE: Osteoarthritis (OA) is a progressive disease characterized by degeneration of cartilage and echinacoside (Ech) has anti-inflammatory and antioxidant effects in various human diseases. This study aimed to reveal the effect and potential mechanism of Ech on OA.
MATERIALS AND METHODS: The in vitro OA model was established by rat chondrocytes treated with IL-1β, and the in vivo OA model was established by anterior cruciate ligament transaction. The effect of Ech on the viability, inflammatory response, extracellular matrix (ECM) degradation, and oxidative stress of IL-1β-treated rat chondrocytes were evaluated by Cell Counting Kit-8 assay, enzyme-linked immunosorbent assay, quantitative real-time PCR, Western blot, and immunofluorescence assay. Meanwhile, the mechanism of Ech was assessed using Western blot, Cell Counting Kit-8 assay, enzyme-linked immunosorbent assay, and immunofluorescence analysis. Moreover, the function of Ech in vivo was analyzed in rat models of OA.
RESULTS: Functionally, Ech enhanced the viability of rat chondrocytes, repressed the inflammatory response and ECM degradation of rat chondrocytes induced by IL-1β with restrained oxidative stress. Mechanically, Ech repressed IL-1β-induced chondrocyte injury by activating the Nrf2/HO-1 signaling pathway. Meanwhile, Ech alleviated the degree of articular cartilage injury in rats and exerted protective effects on the rat model of OA in vivo.
DISCUSSION AND CONCLUSIONS: Ech alleviated OA in rats by activating the Nrf2-HO-1 signaling pathway.
MATERIALS AND METHODS: The in vitro OA model was established by rat chondrocytes treated with IL-1β, and the in vivo OA model was established by anterior cruciate ligament transaction. The effect of Ech on the viability, inflammatory response, extracellular matrix (ECM) degradation, and oxidative stress of IL-1β-treated rat chondrocytes were evaluated by Cell Counting Kit-8 assay, enzyme-linked immunosorbent assay, quantitative real-time PCR, Western blot, and immunofluorescence assay. Meanwhile, the mechanism of Ech was assessed using Western blot, Cell Counting Kit-8 assay, enzyme-linked immunosorbent assay, and immunofluorescence analysis. Moreover, the function of Ech in vivo was analyzed in rat models of OA.
RESULTS: Functionally, Ech enhanced the viability of rat chondrocytes, repressed the inflammatory response and ECM degradation of rat chondrocytes induced by IL-1β with restrained oxidative stress. Mechanically, Ech repressed IL-1β-induced chondrocyte injury by activating the Nrf2/HO-1 signaling pathway. Meanwhile, Ech alleviated the degree of articular cartilage injury in rats and exerted protective effects on the rat model of OA in vivo.
DISCUSSION AND CONCLUSIONS: Ech alleviated OA in rats by activating the Nrf2-HO-1 signaling pathway.