黄芩素通过上调 microRNA-145 保护人视网膜色素上皮细胞系免受高糖诱导的细胞损伤。
Baicalin protects human retinal pigment epithelial cell lines against high glucose-induced cell injury by up-regulation of microRNA-145.
机构信息
Department of Ophthalmology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China; Department of Ophthalmology, Yantai Affiliated Hospital of Binzhou Medical University, Yantai 264100, China.
Department of Ophthalmology, Yantai Affiliated Hospital of Binzhou Medical University, Yantai 264100, China.
出版信息
Exp Mol Pathol. 2019 Feb;106:123-130. doi: 10.1016/j.yexmp.2019.01.002. Epub 2019 Jan 6.
BACKGROUND
Diabetic retinopathy (DR) is a common complication of diabetes mellitus, which is a major reason of blindness. Baicalin (BAI) is a flavonoid extracted from Scutellaria baicalensis, whose pharmacological characterizes have been widely reported in various diseases. However, it remains unclear the effect of BAI on DR. The study aimed to confirm the protective effect of BAI on DR.
METHODS
ARPE-19 cells and HRMECs were exposed to the high glucose (HG) environment to construct a cell injury model. After treatment with HG and BAI, cell viability, apoptosis, inflammatory cytokines and ROS generations were determined in ARPE-19 cells and HRMECs. Subsequently, microRNA-145 (miR-145) inhibitor and its negative control were transfected into ARPE-19 cells, and the regulatory effects on HG-and BAI-co-treated cells were detected. NF-κB and p38MAPK signaling pathways were finally examined to state the underling mechanisms.
RESULTS
HG treatment significantly induced ARPE-19 cells and HRMECs injury in vitro. BAI significantly promoted cell proliferation, reduced apoptosis, as well as inhibited the release of IL-1β, IL-6, IL-8 and ROS level in HG-injured ARPE-19 cells and HRMECs. Additionally, the expression level of miR-145 was up-regulated in HG-and BAI-co-treated cells. More importantly, miR-145 inhibition reversed the protective effect of BAI on HG-injured ARPE-19 cells. Besides, we observed that BAI inhibited the activations of NF-κB and p38MAPK pathways by up-regulating miR-145.
CONCLUSIONS
Results demonstrated that BAI exhibited the protective effect against HG-induced cell injury by up-regulation of miR-145.
背景
糖尿病视网膜病变（DR）是糖尿病的常见并发症，也是失明的主要原因。黄芩苷（BAI）是从黄芩中提取的一种黄酮类化合物，其在各种疾病中的药理作用已被广泛报道。然而，BAI 对 DR 的影响尚不清楚。本研究旨在证实 BAI 对 DR 的保护作用。
方法
将 ARPE-19 细胞和 HRMECs 暴露于高糖（HG）环境中，构建细胞损伤模型。在 HG 和 BAI 处理后，测定 ARPE-19 细胞和 HRMECs 的细胞活力、细胞凋亡、炎症细胞因子和 ROS 生成。随后，将 microRNA-145（miR-145）抑制剂及其阴性对照转染到 ARPE-19 细胞中，检测其对 HG 和 BAI 共处理细胞的调节作用。最后，检测 NF-κB 和 p38MAPK 信号通路，以阐明潜在机制。
结果
HG 处理显著诱导 ARPE-19 细胞和 HRMECs 体外损伤。BAI 显著促进细胞增殖，减少凋亡，并抑制 HG 损伤的 ARPE-19 细胞和 HRMECs 中 IL-1β、IL-6、IL-8 和 ROS 水平的释放。此外，miR-145 在 HG 和 BAI 共处理的细胞中的表达水平上调。更重要的是，miR-145 抑制逆转了 BAI 对 HG 损伤的 ARPE-19 细胞的保护作用。此外，我们观察到 BAI 通过上调 miR-145 抑制 NF-κB 和 p38MAPK 通路的激活。
结论
结果表明，BAI 通过上调 miR-145 发挥对 HG 诱导的细胞损伤的保护作用。
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