A photobiomodulation method for improving high glucose-induced injury of human renal tubular epithelial cells and application thereof
By treating high-glucose-induced human renal tubular epithelial cells with specific photobiological regulation parameters, the problem of effective intervention for renal fibrosis in existing technologies has been solved, cell proliferation and migration capabilities have been improved, related signaling pathways have been inhibited, and the progression of diabetic nephropathy has been delayed.
Patent Information
- Authority / Receiving Office
- CN · China
- Patent Type
- Applications(China)
- Current Assignee / Owner
- NINGBO MEDICAL CENT LIHUILI HOSPITACL
- Filing Date
- 2026-06-24
- Publication Date
- 2026-07-24
AI Technical Summary
Existing technologies cannot effectively target and repair damaged high-glucose-induced human renal tubular epithelial cells, and the application of existing photobiological regulation therapy in DKD has not yet formed a standardized intervention system, lacking effective intervention methods for renal fibrosis.
High glucose-induced human renal tubular epithelial cells were treated with specific light parameters (590nm–1050nm), energy density (4–10J/cm2), and power density (30–50mw/cm2) to regulate oxidative stress, inflammatory response, and apoptosis. Cell proliferation and migration were improved by downregulating the interstitial fibrosis marker α-SMA, upregulating E-cadherin expression, and inhibiting the PI3K/AKT/Smad2 signaling pathway.
It significantly improves the proliferation and migration of renal tubular epithelial cells induced by high glucose, downregulates interstitial fibrosis markers, inhibits the PI3K/AKT/Smad2 signaling pathway, blocks renal tubular epithelial cell damage, and delays the progression of diabetic nephropathy.
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