为研究杨梅酮的抗氧化和抗膀胱癌活性，进行了抗氧化试验和环境扫描电子显 微镜( ESEM) 观察． 结果表明，杨梅酮能有效抑制 AAPH 诱导的红细胞溶血，且效果呈浓 度依赖性，80 μmol /L 杨梅酮的溶血抑制率达到( 93． 67 ± 0． 01) % ． 研究表明，杨梅酮可通 过增强细胞内 SOD、GPx 的酶活来调控 ＲOS 水平，减少 MDA 产生，避免脂质过氧化． 抗肿 瘤活性研究发现，杨梅酮对膀胱癌细胞 EJ 和 T24 以及正常膀胱细胞 SV-HUC-1 的抑制效 果也有剂量相关性，IC50分别为( 39． 8 ± 1． 0) 、( 49． 0 ± 0． 9) 、( 75． 9 ± 1． 8) μmol /L． 进一步 细胞吸收量分析表明，可能是 EJ 对杨梅酮有更强的细胞吸收导致了杨梅酮对 EJ 的 IC50 比 T24 更低( 更敏感的细胞毒性) ． 采用流式细胞术分析杨梅酮对 EJ 细胞周期 DNA 分布 的影响，发现杨梅酮主要通过诱导 EJ 细胞产生凋亡及 S 期阻滞抑制细胞增殖．

Antioxidant assay and ESEM observation were carried out to investigate the antioxidant and anti-bladder cancer activities of myricetin． The results show that myricetin can effectively inhibit the AAPH-induced hemolysis of erythrocytes in a dose-dependent manner． The hemolysis inhibition rate of myricetin increases to ( 93. 67 ± 0. 01) % at a concentration of 80 μmol /L． A further experiment confirms that SOD and GPx antioxidant enzyme activities are enhanced to control ＲOS and MDA generation when erythrocytes are preconditioned by myricetin． Moreover，MTT tests indicate that myricetin could suppress the EJ and T24 bladder cancer cells proliferation in a dose-related manner with the half-maximal inhibitory concentration ( IC50 ) of ( 39. 8 ± 1. 0) μmol /L and ( 49. 0 ± 0. 9) μmol /L，as well as a lower cytotoxicity on normal bladder cell SV-HUC-1 with the IC50 of ( 75. 9 ± 1. 8) μmol /L． In addition， myricetin exhibits higher antitumor activity in EJ cell than that in T24 cells due to higher intracellular uptake amount of myricetin in EJ cells． Further flow cytometric studies of EJ cell cycle distribution show that myricetin inhibits the proliferation of EJ cancer cells mainly through induction of apoptosis and S cycle arrest．