To investigate the effect of GSRd on apoptosis after MCAO, the cleaved caspase-3 was measured by Western blotting analysis [Figure 2]a and [Figure 2]b.
Using RAMF, the mtDNA and nDNA damages were evaluated and quantitated by RT-PCR in the MCAO and MCAO + GSRd groups [Figure 3].
To evaluate the effect of GSRd administration on the expression of NEIL s, both messenger RNA (mRNA) and protein levels of NEIL were measured in rat ipsilateral cortices and hippocampi at 3 days and 7 days after MCAO [Figure 5].
The previous studies showed that GSRd had a neuroprotective function in ischemic stroke.[sup], In the present study, we investigated the effects of GSRd on the expression of DNA glycosylase NEILs in a rat MCAO model.
Our previous work has revealed that GSRd is a neuroprotective agent through ameliorating oxidative stress after ischemic stroke.[sup], Similar results were observed in another study wherein oxidative stress was suppressed by GSRd pretreatment in the dopamine-induced apoptosis PC12 cell model.[sup] In seeking to further explore the neuroprotective mechanism of GSRd after ischemic stroke, we found that GSRd upregulated the expression of NEIL1 in the cortex at 3 days after MCAO and NEIL3 in the hippocampus at 7 days after MCAO in a rat model.
Neural stem/progenitor cells from aged NEIL3 gene knockout mice showed impaired proliferative capacity and reduced DNA repair activity, indicating that NEIL3 was critical in maintaining hippocampal neurogenesis.[sup], Our previous studies found that GSRd promoted neurogenesis in vitro and in vivo [sup] and also showed the ability to maintain neural stem cell proliferation in a lead exposure rat model.[sup] In this study, we found that GSRd-induced NEIL3 expression in the hippocampus could be one of the mechanisms contributing to neurogenesis promotion, leading to the improvement of survival rates and neurological scores in GSRd-treated MCAO rats.