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SMP30 May protect human lens epithelial cells against high glucose-induced oxidative damage by regulating the
Yingqin Yang1, Hongtao Chai2, Tian Lan3
1Department of Ophthalmology, The First Affiliated Hospital of Guilin Medical University, Guangxi Zhuang Autonomous Region, Guilin, 541000, China.
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.
Insights
This study reveals that SMP30 protects against high glucose-induced oxidative stress in diabetic cataract patients by regulating the Keap1/Nrf2/NQO1 pathway. Overexpressing SMP30 enhances cell viability and reduces damage in lens cells.
Area of Science:
- Ophthalmology
- Endocrinology
- Molecular Biology
Background:
- Diabetic cataract (DC) is a significant complication of diabetes mellitus.
- Understanding the molecular mechanisms underlying DC is crucial for developing effective treatments.
- The role of SMP30 in high glucose-induced oxidative stress in lens epithelial cells remains unclear.
Purpose of the Study:
- To investigate the role and mechanism of SMP30 in diabetic cataract patients.
- To explore SMP30's function in high glucose-stimulated human lens epithelial cells (HLE-B3).
- To elucidate the involvement of the Keap1/Nrf2/NQO1 pathway in SMP30's protective effects.
Main Methods:
- Collected aqueous humor and lens anterior capsules from DC patients.
- Stimulated HLE-B3 cells with varying glucose concentrations.
- Transfected HLE-B3 cells with SMP30-overexpressing plasmids.
- Assessed oxidative stress markers (SOD, MDA, ROS), cell viability, and gene/protein expression of SMP30 and Keap1/Nrf2/NQO1 pathway factors.
Main Results:
- Poor glycemic control in DC patients correlated with increased blood/aqueous humor glucose, elevated MDA, decreased SOD, and upregulated SMP30 expression.
- High glucose (40 mM, 60 mM) induced oxidative stress in HLE-B3 cells, with SMP30 downregulation and Keap1/Nrf2/NQO1 pathway inhibition at higher concentrations.
- Overexpression of SMP30 mitigated high glucose-induced oxidative stress, enhanced cell viability, and modulated the Keap1/Nrf2/NQO1 pathway.
Conclusions:
- SMP30 plays a protective role against high glucose-induced oxidative stress in human lens epithelial cells.
- SMP30's protective mechanism involves the regulation of the Keap1/Nrf2/NQO1 pathway.
- Targeting SMP30 may offer a therapeutic strategy for preventing or treating diabetic cataracts.
