Abstract

We have previously reported that syringic acid (SA) extracted from D. aurantiacum var. denneanum (kerr) may be used to prevent diabetic cataract (DC). However, the underlying mechanisms through which SA prevents DC in human lens epithelial cells (HLECs) remained unclear. In the present study, we employed single-molecule optics technologies, including transmission electron microscopy (TEM), atomic force microscopy (AFM), laser scanning confocal microscopy (LSCM) and Raman spectroscopy, to monitor the effect of SA on HLECs biomechanics and organelle structure in real-time. TEM suggested that SA improved the ultrastructure of HLECs with regard to nuclear chromatin condensation and reducing mitochondrial swelling and degeneration, which may aid in the maintenance of HLECs integrity in the presence of glucose. AFM revealed a reduced surface roughness and stiffness following SA treatment, suggesting an improved viscoelasticity of HELCs. Raman spectrometry and LSCM further revealed that these changes were related to a modification of cell liquidity and cytoskeletal structure by SA. Taken together, these results provide insights into the effects of SA on the biomechanics of HLECs and further strengthen the evidence for its potential use as a novel therapeutic strategy for DC prevention.

Highlights

  • Cataract is a primary cause of visual impairment in diabetic patients and, due to the rising incidence of diabetes, diabetic cataract (DC) constitutes an emerging global health problem (Abdel-Ghaffar et al 2018; Goutham et al 2017; Hwang et al 2019; Peterson et al 2018)

  • Minimum essential medium (MEM), phosphate buffered solution (PBS) and penicillin-streptomycin and 0.25% trypsin were purchased from Gibco (Grand Island, NY, USA); fetal bovine serum (FBS) was purchased from Biological Industries (Beit Haemek, Israel); glucose was purchased from Aladdin Industrial Corporation (Shang Hai, China); rhodamine was purchased from Enzo Life Sicences (Farmingdale, NY, USA); DAPI (4′,6-diamidino-2-phenylindole) was purchased from Yeasen (Shanghai, China); triton-100 was purchased from Dingguo Changsheng biotech Co

  • As we demonstrated by Raman spectroscopy and laser scanning confocal microscopy (LSCM), the membrane lipid structure and F-actin organization in the cytoskeleton of human lens epithelial cells (HLECs) was disrupted by high glucose concentrations, but could be rescued by syringic acid (SA) treatment

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Summary

Introduction

Cataract is a primary cause of visual impairment in diabetic patients and, due to the rising incidence of diabetes, diabetic cataract (DC) constitutes an emerging global health problem (Abdel-Ghaffar et al 2018; Goutham et al 2017; Hwang et al 2019; Peterson et al 2018). Previous research findings suggest that during the development of DC, several pathological processes occur, including, an increased osmotic pressure due to an activation of the polyol pathway, an imbalance of redox state due to disruptions of the oxidative stress pathway, and an accumulation of advanced glycation end-products in the glycosylation pathway. These processes result in the breakdown of cellular structure and disrupt the intracellular homeostasis of LECs (Bhadada et al 2016; Obrosova et al 2010), resulting in opacification of the lens (Yang and Zhang 2015). Proliferation and migration of LECs have been observed after cataract surgery and have been suggested to cause capsular opacity and other postoperative complications (Wertheimer et al 2014; Choi et al 2012)

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