Background
Diabetes retinopathy (DR) is a chronic, progressive, and potentially harmful retinal disease associated with persistent hyperglycemia. Autophagy is a lysosome-dependent degradation pathway that widely exists in eukaryotic cells, which has recently been demonstrated to participate in the DR development. Stachydrine (STA) is a water-soluble alkaloid extracted from Leonurus heterophyllus. This study aimed to explore the effects of STA on the autophagy in DR progression in vivo and in vitro.
Conclusion
In conclusion, this study demonstrated that STA effectively relieved the inflammation and promoted the autophagy in DR progression in vivo and in vitro through activating the AMPK/SIRT1 signaling pathway.
Methods
High glucose-treated human retinal microvascular endothelial cells (HRMECs) and STA-treated rats were used to establish DR model. The reactive oxygen species (ROS) and inflammatory factor levels (TNF-α, IL-1β, and IL-6) were determined using corresponding kits. Additionally, the cell growth was analyzed using CCK-8 and EdU assays. Besides, LC3BII, p62, p-AMPKα, AMPKα, and SIRT1 protein levels were measured using Western blot. The LC3BII and SIRT1 expressions were also determined using immunofluorescence.
Results
The results showed that STZ decreased the ROS and inflammatory factor levels in the HG-treated HRMECs. Besides, after STA treatment, the beclin-1, LC3BII, p-AMPKα, and SIRT1 levels were increased, and p62 was decreased in the HG-treated HRMECs and the retinal tissue of STZ-treated rats.