Department of Orthopaedics, Second Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing 400010, China.
Department One of Orthopedics, Ninth People's Hospital of Chongqing, Chongqing 400700, China.
Appl Physiol Nutr Metab. 2021 Nov;46(11):1331-1336. doi: 10.1139/apnm-2020-0958. Epub 2021 May 14.
The study aimed to investigate the preservative effects of genistein on articular cartilage in an experimental model of knee osteoarthritis in rats. Thirty male Wistar rats were assigned to 3 equal groups: sham group, osteoarthritis control group (OAG), and genistein-treated osteoarthritis group (GTG). Intra-articular injections of monosodium iodoacetate were used for osteoarthritis induction. After 2 weeks of rest for the induction of the inflammatory process, genistein (30 mg/kg/day) vs. saline gavage was administered for 8 weeks. The expression of matrix metalloproteinase and , /, Indian hedgehog (), and were evaluated in medial femoral condyle sections by immunohistochemical staining. The number of chondrocytes and cartilage thicknesses were also measured and compared among the groups. No significant change in cartilage thickness was observed in GTG compared with OAG ( = 0.188). Chondrocyte count was significantly higher in the articular cartilage of GTG compared with OAG ( = 0.006). Induction of osteoarthritis significantly increased the expression of , , and , but decreased , , and expression ( < 0.001); these were partially prevented in the GTG. Our findings support the effectiveness of genistein treatment in the prevention of articular cartilage damage in the experimental model of knee osteoarthritis. The proposed mechanism of action is through the suppression of the , , and pathways, besides the induction of and expression. Genistein prevents articular cartilage damage in the experimental model of knee osteoarthritis. The osteoprotective effect is manifested by the modulation of expression of MMP, Sox, IHH, and Col2 proteins.
本研究旨在探讨染料木黄酮在膝骨关节炎大鼠实验模型中对关节软骨的保护作用。将 30 只雄性 Wistar 大鼠随机分为 3 组：假手术组、骨关节炎对照组（OAG）和染料木黄酮治疗骨关节炎组（GTG）。采用关节内注射单碘乙酸钠诱导骨关节炎。诱导炎症过程 2 周后，给予 GTG（30mg/kg/天）或生理盐水灌胃 8 周。通过免疫组织化学染色评估内侧股骨髁节段中基质金属蛋白酶 13（MMP13）、转化生长因子β1（TGF-β1）、/β、印度刺猬（）和 Col2 的表达。还测量并比较了各组的软骨细胞数量和软骨厚度。与 OAG 相比，GTG 组的软骨厚度无显著变化（=0.188）。与 OAG 相比，GTG 组关节软骨中的软骨细胞计数显著更高（=0.006）。骨关节炎的诱导显著增加了、和的表达，但降低了、和的表达（<0.001）；这些在 GTG 中部分得到预防。我们的研究结果支持染料木黄酮治疗在预防膝骨关节炎实验模型中关节软骨损伤的有效性。其作用机制可能是通过抑制、和途径，以及诱导和表达来实现。染料木黄酮可预防膝骨关节炎实验模型中的关节软骨损伤。其护骨作用表现为调节 MMP、Sox、IHH 和 Col2 蛋白的表达。
