Stachydrine Mitigates High Glucose-Induced Apoptosis In Human Lens Epithelial Cells By Activating Mitophagy
Published 2025 - 43rd Congress of the ESCRS
Reference: PO789 | Type: Free paper | DOI: 10.82333/7xfq-qk63
Authors: Hagay Hayat* 1 , Shawn Sapir 1 , Tzahi Sela 2 , Gur Munzer 2 , Igor Kaiserman 3
1ophthalmology department,Barzilai University Medical Center,Ashkelon,Israel, 2Care-Vision Laser Center,Tel-Aviv,Israel, 3ophthalmology department,Barzilai University Medical Center,Ashkelon,Israel;Care-Vision Laser Center,Tel-Aviv,Israel
Purpose
Recent studies have highlighted the potential protective effects of natural plant extracts in the context of DC. Stachydrine (STA), an alkaloid derived from Leonurus heterophyllus Sweet, has been identified as a natural compound with superior bioavailability and fewer side effects than conventional antioxidants. In this study, we aimed to investigate the protective role of STA on high-glucose-induced lens epithelial cells.
Setting
Tianjin Medical University Eye Hospital, Tianjin, China
Methods
In this study, we established a high-glucose model using HLE-B3 cells and assessed apoptosis following STA treatment. Mitochondrial network morphology was analyzed using the ImageJ software. To further investigate the role of autophagy in STA’s effects, we employed the autophagy inhibitor 3-Methyladenine (3-MA).
Results
Our results indicated that high glucose exposure decreased autophagosome formation and lysosomal activity, while STA treatment significantly increased both. Furthermore, STA enhanced LC3B expression and reduced P62 levels, counteracting the effects of high glucose. Regarding mitochondrial morphology, STA effectively restored the shape, branching, and area, all of which were diminished by high glucose exposure.
Additionally, STA effectively ameliorated mitochondrial network damage induced by high glucose. Notably, when the cells were treated with 3-MA, STA’s protective effects on apoptosis and mitochondrial morphology were significantly reversed.
Conclusions
In conclusion, our findings suggest that STA exerts protective effects against high-glucose-induced damage by regulating mitophagy, and this autophagy-dependent mechanism may hold therapeutic potential for the treatment of diabetic cataract.