Department of Ophthalmology, Second Hospital of Hebei Medical University, No. 215 Peace West Road, Qiaoxi District, Shijiazhuang, Hebei, 050000, China.
Department of Ophthalmology, Cangzhou Central Hospital, No. 16 Xinhua West Road, Cangzhou, Hebei, 061000, China.
BMC Complement Altern Med. 2018 Mar 13;18(1):89. doi: 10.1186/s12906-018-2155-3.
This study aimed to explore the effects of plumbagin (PLB) on ARPE-19 cells and underlying mechanism.
Cultured ARPE-19 cells were treated with various concentrations (0, 5, 15, and 25 μM) of PLB for 24 h or with 15 μM PLB for 12, 24 and 48 h. Then cell viability was evaluated by MTT assay and DAPI staining, while apoptosis and cell cycle progression of ARPE cells were assessed by flow cytometric analysis. Furthermore, the level of main regulatory proteins was examinated by Western boltting and the expression of relative mRNA was tested by Real-Time PCR.
PLB exhibited potent inducing effects on cell cycle arrest at G2/M phase and apoptosis of ARPE cells via the modulation of Bcl-2 family regulators in a concentration- and time-dependent manner. PLB induced inhibition of phosphatidylinositol 3-kinase (PI3K) and p38 mitogen-activated protein kinase (p38 MAPK) signaling pathways contributing to the anti-proliferative activities in ARPE cells.
This is the first report to show that PLB could inhibit the proliferation of RPE cells through down-regulation of modulatory signaling pathways. The results open new avenues for the use of PLB in prevention and treatment of proliferative vitreoretinopathy.
本研究旨在探讨白花丹醌（PLB）对 ARPE-19 细胞的作用及其机制。
用不同浓度（0、5、15 和 25μM）PLB 处理 ARPE-19 细胞 24h 或用 15μM PLB 处理 12、24 和 48h。然后用 MTT 法和 DAPI 染色评估细胞活力，用流式细胞术分析 ARPE 细胞的凋亡和细胞周期进程。此外，通过 Western blot 检测主要调节蛋白的水平，通过 Real-Time PCR 检测相对 mRNA 的表达。
PLB 通过调节 Bcl-2 家族调节剂，以浓度和时间依赖的方式对 ARPE 细胞的细胞周期阻滞在 G2/M 期和凋亡具有很强的诱导作用。PLB 诱导磷脂酰肌醇 3-激酶（PI3K）和 p38 丝裂原活化蛋白激酶（p38 MAPK）信号通路的抑制，从而抑制 ARPE 细胞的增殖活性。
这是首次报道 PLB 可通过下调调节信号通路抑制 RPE 细胞的增殖。这些结果为 PLB 在预防和治疗增生性玻璃体视网膜病变中的应用开辟了新的途径。
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