Emodin Attenuates the ECM Degradation and Oxidative Stress of Chondrocytes through the Nrf2/NQO1/HO-1 Pathway to Ameliorate Rat Osteoarthritis

Figure 6

Progression of OA in rats induced by ACLT with or without emodin. (a) Macroscopic image and (b) Pelletier score of the rat knee joint 6 weeks after emodin administration. (c, e) The cartilage surface of the femoral condyle and tibial plateau of the control group was smooth without cartilage defects. Rats in the untreated OA group showed severe cartilage damage, the middle layer of cartilage was eroded, and the subchondral bone was exposed. Cartilage loss after emodin treatment is improved, and the degree of ulcers on the cartilage surface is reduced. After 6 weeks of emodin treatment, hematoxylin-eosin (HE) staining, Safranin O staining (scale bar: 200 μm), and (d, f) OARSI score representative knee joint images. In the control group, chondrocytes had no vacuoles and Safranin O stained evenly. In the OA group, chondrocytes were severely damaged, chondrocytes were hypertrophy, and chondrocytes aggregated. After six weeks of treatment, emodin can improve the loss of chondrocytes and inhibit the loss of proteoglycan in ECM. The data are presented as the (). .

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