目的：探讨紫檀芪对高糖环境下诱导的人视网膜微血管内皮细胞(HRMECs)内皮间充质转化(EndMT)的潜在抑制作用。

方法：采用CCK-8测定法确定紫檀芪处理HRMECs的最适浓度，选择了12.5、25 μmol/L的浓度进行后续实验。将HRMECs分为对照组、高糖组、高糖联合12.5 μmol/L紫檀芪处理组以及高糖联合25 μmol/L紫檀芪处理组。通过Western blot法检测各组细胞中HDAC7表达以及与EndMT相关的标志蛋白水平； Transwell迁移实验和划痕愈合实验评估各组细胞的迁移能力； 管腔形成实验用于评价细胞的血管生成能力。

结果：CCK-8实验结果表明紫檀芪在22.07 μmol/L浓度时能将HRMECs细胞活性抑制50%。Western blot分析显示，相较于对照组，高糖培养的HRMECs中HDAC7、ZEB1、Vimentin和Snail的表达水平显著升高(均P<0.01)，而VE-cadherin和CD31的表达显著降低(均P<0.01)。相较于高糖组，12.5、25 μmol/L紫檀芪的处理能够显著降低高糖条件下的HDAC7、ZEB1、Vimentin和Snail的表达(均P<0.01)，25 μmol/L紫檀芪能够增强VE-cadherin和CD31的表达(均P<0.01)。划痕实验结果显示，高糖处理组的HRMECs显示出较对照组显著增加的细胞迁移率(P<0.05)，而25 μmol/L紫檀芪的应用均显著抑制了HRMECs在高糖条件下的细胞迁移(P<0.01)。Transwell迁移实验结果显示，高糖组的细胞迁移率显著高于对照组(P<0.01)，且12.5、25 μmol/L紫檀芪处理后细胞迁移率较高糖组明显降低(均P<0.01)。管腔形成实验表明，高糖环境下HRMECs的管腔形成能力显著增强(P<0.01)，并且12.5、25 μmol/L紫檀芪均能有效抑制这一效应(均P<0.01)。

结论：紫檀芪能抑制高糖介导的HRMECs的EndMT及HDAC7的表达，并抑制细胞迁移及管腔形成能力。

METHODS: The optimal concentration of pterostilbene for treating HRMECs was determined using the CCK-8 assay, with 12.5 and 25 μmol/L concentrations selected for subsequent experiments. Four experimental groups were established: control group, high glucose group, high glucose combined with 12.5 μmol/L pterostilbene treatment group, and high glucose combined with 25 μmol/L pterostilbene treatment group. The expression levels of HDAC7 and EndMT-associated markers were detected via Western blot analysis. Cell migration ability was assessed using Transwell migration assays and scratch wound healing tests, while vasculogenic capability was evaluated through tube formation assays.

RESULTS: The CCK-8 assay revealed that pterostilbene at a concentration of 22.07 μmol/L inhibited 50% of cell viability in HRMECs. Western blot analysis demonstrated that compared with the control group, the expression levels of HDAC7, ZEB1, Vimentin, and Snail were significantly upregulated in HRMECs cultured in high glucose(all P<0.01), while the expressions of VE-cadherin and CD31 were significantly reduced(all P<0.01). Compared to the high glucose group, the treatment with 12.5 and 25 μmol/L pterostilbene significantly reduced the expression of HDAC7, ZEB1, Vimentin, and Snail under high glucose conditions(all P<0.01). Notably, 25 μmol/L pterostilbene enhanced the expression of VE-cadherin and CD31(all P<0.01). Scratch wound healing tests revealed that HRMECs treated with high glucose exhibited a significantly increased cell migration rate compared to the control group(P<0.05), while the application of 25 μmol/L pterostilbene significantly suppressed HRMECs migration under high glucose conditions(P<0.01). Transwell migration assays demonstrated that the cell migration rate in the high glucose group was significantly higher than that in the control group(P<0.01), with cell migration rate markedly reduced following treatment with both of 12.5 and 25 μmol/L pterostilbene(all P<0.01). The tube formation assay revealed that the ability of HRMECs to form tubular structures was significantly enhanced under high glucose conditions(P<0.01), and both 12.5 and 25 μmol/L of pterostilbene effectively inhibited this effect(all P<0.01).

CONCLUSION: Pterostilbene can inhibit HDAC7 expression, suppress EndMT-mediated migration of HRMECs, and impair tube formation under high-glucose conditions.