Erschienen in:
01.12.2024 | Original Paper
PD protects Müller cells through the SIRT1/NLRP3 inflammasome pathway
verfasst von:
Bing Wang, Xiaoyu Qu, Anle Su, Hongna Zhu
Erschienen in:
International Ophthalmology
|
Ausgabe 1/2024
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Abstract
Purpose
Polydatin (PD) has widely pharmacological activities. However, the effects of PD on high glucose (HG)-induced Müller cells in diabetic retinopathy (DR) are rarely studied.
Methods
The protective effects of PD were evaluated in HG-induced human retinal Müller cells. The levels of pro-angiogenic factors and pro-inflammatory factors were detected using the ELISA kits. The expressions of nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing-3 (NLRP3) and sirtuin-1 (SIRT1) were determined by western blot.
Results
PD inhibited proliferation and activation of HG-induced MIO-M1 cells. PD treatment reduced the levels of pro-angiogenic factors, pro-inflammatory factors, and oxidative stress, while these effects were attenuated by NLRP3 agonist ATP in HG-induced MIO-M1 cells. Furthermore, PD inhibited the activation of NLRP3 inflammasome by regulating the SIRT1 expression after HG stimulation, and knockdown of SIRT1 reversed the inhibition effects of PD on NLRP3 inflammasome, pro-angiogenic factors, pro-inflammatory factors, and oxidative stress in HG-induced MIO-M1 cells.
Conclusion
PD may inhibit HG-induced Müller cells proliferation and activation and suppress pro-angiogenic factors, pro-inflammatory factors, and oxidative stress through the SIRT1/NLRP3 inflammasome pathway. In summary, PD treatment may be an effective therapeutic strategy for DR.