KOA常表现为反复的关节疼痛和逐渐恶化的关节功能障碍。它是目前临床常见的慢性进行性退行性骨关节病之一，疾病持续时间长且容易复发。探索KOI的新治疗方法和机制对于治疗KOI至关重要。钠透明质酸（SH）在医学领域中的主要应用之一是治疗骨性关节炎。然而，SH单独治疗KOI的效果有限。羟基藏红花黄素A（HSYA）可能对KOI具有治疗作用。本研究旨在调查HSYA+SH治疗KOI兔软骨组织的治疗效果和可能的作用机制，并为KOI的治疗提供理论依据。研究小组进行了动物实验。该研究在中国辽宁省沈阳市辽宁集家生物技术有限公司进行。动物是30只健康的成年新西兰白兔，体重为2-3kg。研究小组将兔随机分成三组，每组10只：（1）对照组，研究小组未诱导KOI并未提供治疗；（2）HSYA+SH组，干预组，研究小组诱导KOI并注射兔子HSYA+SH治疗；（3）KOA组，研究小组诱导KOI并注射盐水兔子。研究小组：（1）使用苏木精-伊红（HE）染色观察软骨组织形态学变化；（2）使用酶联免疫吸附法（ELISA）测量血清炎性因子水平，包括肿瘤坏死因子α（TNF-α）、白细胞介素-1β（IL-1β）、干扰素γ（IFN-γ）、IL-6和IL-17；（3）使用“末端脱氧核苷酸转移酶（TdT）dUTP末端标记”（TUNEL）测量软骨细胞凋亡；（4）使用Western Blot检测与“神经发生位点切割同源蛋白1”（Notch1）信号通路相关的蛋白质表达。与对照组相比，KOA组的软骨组织发生了形态学变化。与对照组相比，该组的细胞凋亡率较高，血清炎性因子水平显著升高（P <0.05），与Notch1信号通路相关的蛋白质表达也显著升高（P <0.05）。HSYA+SH组的软骨组织形态比KOA组好但不如对照组。与KOA组相比，HSYA+SH组的细胞凋亡率较低，血清炎性因子水平显著降低（P<0.05），与Notch1信号通路相关的蛋白质表达也显著降低（P<0.05）。HSYA+SH能够减少KOI兔软骨组织的细胞凋亡，降低炎性因子水平，保护兔KOI引起的软骨组织损伤，并且机制可能与调节Notch1信号通路有关。

KOA characterized by recurrent joint pain and progressive joint dysfunction. Is the present clinical common chronic progressive degenerative osteoarthropathy, how long the disease is difficult to cure and easy to relapse. Exploring new therapeutic approaches and mechanisms is important for the treatment of KOA. One of the main applications for sodium hyaluronate (SH) in the medical field is treatment of osteoarthritis. However, the effects of SH alone in the treatment of KOA are limited. Hydroxysafflor yellow A (HSYA) may have therapeutic effects for KOA.The study intended to investigate the therapeutic effects and possible mechanisms of action HSYA+SH for cartilage tissue of rabbits with KOA and to provide a theoretical basis for the treatment of KOA.The research team performed an animal study.The study that took place at Liaoning Jijia Biotechnology, Shenyang, Liaoning, China.The animals were 30 healthy, adult, New Zealand white rabbits, weighing 2-3 kg.The research team randomly divided the rabbits into three groups, with 10 rabbits in each group: (1) a control group, for which the research team didn't induce KOA and provided no treatment; (2) the HSYA+SH group, the intervention group, for which the research team induced KOA and injected the rabbits with the HSYA+SH treatment; and (3) the KOA group, for which the research team induced KOA and injected the rabbits with saline.The research team: (1) observed the morphological changes in the cartilage tissue using hematoxylin-eosin (HE) staining; (2) measured levels of serum inflammatory factors, including tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), interferon gamma (IFN-γ), IL-6, and IL-17 using an enzyme-linked immunosorbent assay (ELISA); (3) measured cartilage-cell apoptosis using "terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling" (TUNEL); and (4) used Western Blot to detect the expression of proteins related to the "neurogenic locus notch homolog protein 1" (Notch1) signaling pathway.Compared with the control group, morphological changes had occurred to the cartilage tissue in the KOA group. Compared with the control group, that group's level of apoptosis was higher, the levels of serum inflammatory factors were significantly higher (P < .05), and the protein expression related to the Notch1 signaling pathway was also significantly higher (P < .05). The morphology of the cartilage tissue in the HSYA+SH was better than that of the KOA group but not as good as that of the control group. Compared with the KOA group, the HSYA+SH group's level of apoptosis was lower, the levels of serum inflammatory factors were significantly lower (P < .05), and the protein expression related to the Notch1 signaling pathway was also significantly lower (P < .05).HSYA+SH can reduce the cellular apoptosis in the cartilage tissue of rabbits with KOA, downregulate the levels of inflammatory factors, and protect against KOA-induced cartilage tissue injury, and the mechanism may be related to the regulation of the Notch1 signaling pathway.