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Sulforaphane alleviates retinal ganglion cell death and inflammation by suppressing NLRP3 inflammasome activation in a rat model of retinal ischemia/reperfusion injury
Author(s) -
Gong Yuerong,
Cao Xiaoning,
Gong Lei,
Li Weiguo
Publication year - 2019
Publication title -
international journal of immunopathology and pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.724
H-Index - 53
eISSN - 2058-7384
pISSN - 0394-6320
DOI - 10.1177/2058738419861777
Subject(s) - retinal , inflammasome , neuroprotection , microglia , retinal ganglion cell , retina , reperfusion injury , chemistry , inflammation , programmed cell death , pharmacology , gene knockdown , ischemia , microbiology and biotechnology , medicine , biology , immunology , biochemistry , neuroscience , apoptosis
This study aims to study the potentials of sulforaphane (SFN) against retinal ischemia/reperfusion (I/R) injury. A rat retinal I/R injury method was established. Retinal thickness change and retinal ganglion cell (RGC) death were determined using hematoxylin and eosin (H&E) staining and Fluoro-Gold (FG) labeling. The inflammatory cytokines production and microglia activation were evaluated by using quantitative real-time polymerase chain reaction (qRT-PCR), Western blot, and enzyme-linked immunosorbent assay (ELISA). Knockdown NLRP3 was performed, and the according changes of retinal RGCs were assessed. SFN administration significantly inhibited I/R and caused retinal thickness change and prevented RGCs death in retinal I/R model. SFN suppressed inflammatory cytokines production, microglia activation, and inflammasome activation. In accordance, NLRP3 knockdown presented the similar inhibitory effect on I/R rats. This study demonstrates that SFN prevents RGCs death and acts as a potent neuroprotective modulator in retinal I/R injury, which may be associated with inhibition of the NLRP3 inflammasome activation.

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