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Updated: May 27, 2025
A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure
Published on: July 14, 2016
Astragalus polysaccharide attenuates retinal ischemia reperfusion-induced microglial activation through
Juanjuan Li1, Hua Li1, Chunling Wei1
1Department of Ophthalmologic, The Affiliated Hospital of Yunnan University (Second People's Hospital of Yunnan Province, Yunnan Eye Hospital), Kunming, Yunnan, China.
Objective:
Microglial activation is a hallmark of pathogenic retinal conditions such as retinal ischemia-reperfusion (RIR). While sortilin-related vacuolar protein sorting 10 domain containing receptor 2 (Sorcs2) and laminin subunit alpha 1 (Lama1) have been implicated in neuroinflammatory processes, their roles in regulating microglial activation in RIR are not reported. The current work studied the potential of Sorcs2 and Lama1 as negative regulators of microglial activation in RIR and assessed the therapeutic potential of Astragalus polysaccharide (AP).
Material And Methods:
Transcriptome profiling was conducted in retinal specimens of RIR group 72 h after RIR induction. Oxygen-glucose deprivation/reperfusion (OGD/R) in rat microglial cells was employed as the cellular induction model of RIR. The functional role of Sorcs2 and Lama1 in dictating microglial activation was investigated in vitro and in vivo using lentivirus-based gene expression. Further, the potential effect of AP on RIR-mediated microglial activation was investigated.
Results:
Sorcs2 and Lama1 were identified as two downregulated genes in retinal samples following RIR. OGD/R induction triggered pro-inflammatory microglial activation and induced the downregulation of Sorcs2 and Lama1. Sorcs2 or Lama1 overexpression hindered OGD/R-induced microglial activation in vitro and attenuated inflammatory expansion of microglia cells in RIR-induced rat retinal samples. AP treatment was able to neutralize the oxidative stress, promote the expression of Sorcs2 and Lama1, and suppress microglial activation.
Conclusion:
Our findings pinpoint Sorcs2 and Lama1 as negative regulators of microglial activation in RIR. AP could be employed as an antioxidant to attenuate microglial activation and ameliorate the inflammatory damages in RIR.
