目的 探讨白藜芦醇（Res）对H₂O₂处理的骨关节炎成纤维样滑膜细胞的影响，并阐明PINK1/Parkin线粒体自噬信号通路在上述影响中的调控机制关系。 方法 从无骨关节炎手术患者关节滑膜提取成纤维样滑膜细胞（FLSs），从骨关节炎手术患者关节滑膜提取成纤维样滑膜细胞（OA-FLSs），并将其分为对照组、实验组，实验组用H₂O₂（5 μmol/L）处理后，应用不同浓度的Res（0、10、20、40、60、80、100 μmol/L）处理，细胞活力测定（CCK-8）检测细胞增殖抑制率，DCFH-DA荧光探针检测细胞活性氧，MitoSOX Red荧光探针检测细胞线粒体活性氧，流式细胞术检测细胞周期，Western blot以及免疫荧光实验检测NLRP3、TNF-α、IL-1β、SOD2、Bax、Bcl-2、BNIP3、LC3B、p62、PINK1、Parkin等蛋白的表达。使用PINK1、Parkin干扰RNA进一步验证PINK1/Parkin线粒体自噬信号通路在Res抑制FLSs异常增殖、炎症和氧化应激中的作用。 结果 Res显著抑制H₂O₂诱导的FLSs活力的增强，且抑制效果与浓度成正比；Res降低了FLSs的异常增殖、炎症和氧化应激水平；Res抑制了NLRP3、TNF-α、Bcl-2、p62蛋白的表达，同时促进SOD2、Bax、BNIP3、LC3B、PINK1、Parkin蛋白的表达；H₂O₂抑制了PINK1/Parkin信号通路，Res则激活了PINK1/Parkin通路；PINK1和Parkin干扰RNA的使用加剧了细胞炎症和氧化应激。 结论 Res通过增加PINK1和Parkin蛋白的表达来激活PINK1/Parkin线粒体自噬信号通路，减轻了H₂O₂诱导的骨关节炎成纤维样滑膜细胞中异常增殖、炎症和氧化应激。

Objective To investigate the effect of resveratrol （Res） on fibroblast-like synovial cells of osteoarthritis treated with H₂O₂， and to clarify the regulatory mechanism relationship of the PINK1/Parkin mitochondrial autophagy signaling pathway in the above effects. Methods Fibroblast-like synovial cells （FLSs） were extracted from the synovial membranes of patients undergoing osteoarthritis surgery and divided into the control group and the experimental group. The experimental group was treated with H₂O₂ （5 μmol/L） and then treated with different concentrations of Res （0， 10， 20， 40， 60， 80， 100 μmol/L）. Cell viability assay （CCK-8） was used to detect the inhibition rate of cell proliferation. Cell reactive oxygen species were detected by DCFH-DA fluorescent probe. Mitochondrial reactive oxygen species were detected by MitoSOX Red fluorescent probe. Cell cycle was detected by flow cytometry. The expressions of proteins such as NLRP3， TNF-α， IL-1β， SOD2， Bax， Bcl-2， BNIP3， LC3B， p62， PINK1 and Parkin were detected by Western blot and immunofluorescence experiments. The role of the PINK1/Parkin mitochondrial autophagy signaling pathway in Res' inhibition of abnormal proliferation， inflammation and oxidative stress in FLSs was further verified using PINK1 and Parkin interfering RNA. Results Res significantly inhibited the enhancement of FLSs activity induced by H₂O₂， and reduced the abnormal proliferation， inflammation and oxidative stress levels of FLSs； Res inhibited the expressions of NLRP3， TNF-α， Bcl-2 and p62 proteins， while promoting the expressions of SOD2， Bax， BNIP3， LC3B， PINK1 and Parkin proteins. H₂O₂ inhibited the PINK1/Parkin signaling pathway， while Res activated the PINK1/Parkin pathway. The use of PINK1 and Parkin interfering RNA exacerbated cellular inflammation and oxidative stress. Conclusion Res activates the PINK1/Parkin mitochondrial autophagy signaling pathway by increasing the expression of PINK1 and Parkin proteins， alleviating abnormal proliferation， inflammation and oxidative stress in fibroblast-like synovial cells of osteoarthritis induced by H₂O₂.