TGCI

AcronymDefinition
TGCIThe Grantsmanship Center
TGCITransient Global Cerebral Ischemia
TGCIThai-German Ceramic Industry, PCL (Thailand)
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In the 200 mg/kg GLE-ischemia group, a few Iba-1-immunoreactive microglia were activated and the ROD was low compared with that in the vehicle-ischemia group [Figure 3]j, [Figure 3]l, and [Figure 3]n; 5 days after TGCI, the ROD was significantly decreased (about 139% of the vehicle-sham group) [Figure 3]n.
In the vehicle-ischemia group, SOD1 immunoreactivity in neurons of the stratum pyramidale decreased with time after TGCI, showing about 79% of the vehicle-sham group 2 days after TGCI and about 43% of the vehicle-sham group 5 days after TGCI [Figure 4]c, [Figure 4]e, and [Figure 4]m.
In the GLE-ischemia group, SOD1 immunoreactivity in neurons of the stratum pyramidale was continuously maintained after TGCI [Figure 4]d, [Figure 4]f, and [Figure 4]m.
In the vehicle-ischemia group, BDNF immunoreactivity in neurons of the stratum pyramidale was significantly decreased (about 58% of the vehicle-sham group) 2 days after TGCI and was very low (about 32% of the vehicle-sham group) 5 days after TGCI [Figure 4]i, [Figure 4]k, and [Figure 4]n.
In the GLE-ischemia group, BDNF immunoreactivity in neurons of the stratum pyramidale was consistently maintained after TGCI [Figure 4]j, [Figure 4]l, and [Figure 4]n.
Therefore, in this study, we examined neuroprotective effects of GLE in a gerbil model of TGCI using NeuN immunohistochemistry and F-J B histofluorescence staining, which are widely used for the histological evaluation of neuronal damage/death in the central nervous system (CNS),[sup][22],[23] and we found that pretreatment with 200 mg/kg of GLE effectively protected pyramidal neurons in the CA1 from ischemic damage following TGCI.
It has been reported that TGCI leads to the proliferation and activation of glial cells including astrocytes and microglia in the ischemic CA1[sup][6],[27] and that activated astrocytes and microglia take part in ischemia-induced inflammatory response through the synthesis and release of diverse neurotoxic substances including pro-inflammatory cytokines and nitric oxide, which contribute to the development of ischemic neuronal damage/death.
sup][37] In addition, it was reported that the overexpression of SOD1 reduced neuronal death in the CA1, following TGCI using transgenic mice and rats.
Therefore, this result suggests that the increased and sustained BDNF expression following pretreatment with GLE in the sham and ischemia groups might contribute to neuroprotective effects of GLE against TGCI.