PD protects Müller cells through the SIRT1/NLRP3 inflammasome pathway.
Int Ophthalmol
; 44(1): 97, 2024 Feb 19.
Article
en En
| MEDLINE
| ID: mdl-38372810
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.Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Estilbenos
/
Retinopatía Diabética
/
Inflamasomas
/
Glucósidos
Límite:
Humans
Idioma:
En
Revista:
Int Ophthalmol
Año:
2024
Tipo del documento:
Article
País de afiliación:
China