SMP30 May protect human lens epithelial cells against high glucose-induced oxidative damage by regulating the Keap1/Nrf2/NQO1 pathway.
SMP30 may influence oxidative stress in lens epithelial cells under high glucose conditions, but the clinical relevance of these findings is uncertain.
Where it sits
this study against the rest of the nad+ (nicotinamide adenine dinucleotide) corpusSummary and findings
This study investigated the role of SMP30 in human lens epithelial cells under high glucose conditions, focusing on oxidative stress markers and the Keap1/Nrf2/NQO1 pathway. Aqueous humor and lens anterior capsules were collected from diabetic cataract patients, and HLE-B3 cells were stimulated with varying glucose concentrations. The findings suggest that SMP30 may influence oxidative stress responses in these cells.
Abstract
The aim of this study was to explore the role and mechanism of SMP30 in diabetic cataract(DC) patients with different glycemic control levels and high glucose-stimulated human lens epithelial cells. First, aqueous humor and lens anterior capsules were collected during cataract surgery. Second, human lens epithelial B3(HLE-B3) cells were stimulated with different glucose concentrations. Then, SMP30-overexpressing plasmids were transfected into HLE-B3 cells. Measured blood and aqueous humor glucose concentrations in cataract patients. Oxidative stress levels was assessed by analyzing SOD, MDA and ROS. The mRNA and protein expression levels of SMP30 and Keap1/Nrf2/NQO1 pathway factors were detected. The cell viability was analyzed. The glucose concentration in blood and aqueous humor increased, and MDA content increased and SOD activity decreased in DC patients with poor glycemia control. However, SMP30 expression was upregulated of these patients, in parallel with the possible activation of Keap1/Nrf2/NQO1 pathway. The MDA content and ROS levels increased, and SOD activity decreased under high glucose(40 mM, 60 mM) in HLE-B3 cells. Meanwhile, SMP30 expression was up-regulated and Keap1/Nrf2/NQO1 pathway was activated at a glucose of 20 mM, but down-regulated and Keap1/Nrf2/NQO1 pathway was inhibited at a glucose of 40 mM or 60 mM. Overexpression of SMP30 reduced the oxidative stress damage and increased the cell viability, and reversed the expression of Keap1/Nrf2/NQO1 pathway factors induced by high glucose in HLE-B3. This study demonstrates that SMP30 may protect human lens epithelial cells from high glucose-stimulated oxidative stress damage and may involves the regulation of Keap1/Nrf2/NQO1 pathway.
Background
The paper addresses the potential oxidative damage to human lens epithelial cells caused by high glucose levels, which is relevant in the context of diabetes-related ocular complications. Previous studies have suggested that oxidative stress plays a significant role in lens cell damage, but the specific mechanisms and protective agents have not been thoroughly explored. This study aims to elucidate the role of SMP30 in mitigating such damage through the Keap1/Nrf2/NQO1 pathway.
Methods
Not reported in abstract.
Results
Not reported in abstract.
Interpretation
Not reported in abstract.
Key findings
- Not reported in abstract.
Limitations
- Not reported in abstract.