PD protects Müller cells through the SIRT1/NLRP3 inflammasome pathway

Area of Science:

• Ophthalmology
• Cell Biology
• Pharmacology

Background:

• Diabetic retinopathy (DR) is a leading cause of vision loss.
• High glucose (HG) induces Müller cell dysfunction, contributing to DR pathogenesis.
• The therapeutic potential of polydatin (PD) in DR remains largely unexplored.

Purpose of the Study:

• To investigate the protective effects of polydatin (PD) on high glucose (HG)-induced human retinal Müller cells.
• To elucidate the underlying molecular mechanisms involving the SIRT1/NLRP3 inflammasome pathway.

Main Methods:

• Human retinal Müller cells (MIO-M1) were exposed to high glucose (HG).
• Polydatin (PD) treatment effects were assessed on cell proliferation and activation.
• Levels of pro-angiogenic, pro-inflammatory factors, and oxidative stress were quantified using ELISA.
• Expressions of NLRP3 inflammasome and SIRT1 were analyzed via western blot.

Main Results:

• Polydatin (PD) inhibited proliferation and activation of HG-induced Müller cells.
• PD treatment significantly reduced pro-angiogenic factors, pro-inflammatory factors, and oxidative stress.
• These protective effects were diminished by NLRP3 agonist and reversed by SIRT1 knockdown.
• PD regulated SIRT1 expression, thereby inhibiting NLRP3 inflammasome activation.

Conclusions:

• Polydatin (PD) demonstrates protective effects against HG-induced Müller cell damage.
• The mechanism involves the SIRT1/NLRP3 inflammasome pathway, modulating inflammation and oxidative stress.
• PD represents a promising therapeutic strategy for managing diabetic retinopathy (DR).