: 41.67 ; NS: 183.33 , p 0.05). The The VGB group hadhad fewer rats with SRS
: 41.67 ; NS: 183.33 , p 0.05). The The VGB group hadhad fewer rats with SRS, Figure 2. VGB-treated rats had fewer spontaneous recurrent seizures. (A) (B) VGB-treated group fewer extreme Caspase 14 Proteins site seizures Figure two. above), as in comparison with the spontaneous (stage 3 and VGB-treated rats had fewer(VGB: 41.67 ;recurrent seizures. 0.05). 0.05). (C) Thegroup had fewer severewith SRS, NS group (VGB: 40 ; NS: p (A) The VGB-treated group had fewer rats mean in comparison with the typical saline group (VGB: 41.67 ; NS: 183.33 , p p (B) The VGB group count of every day seizures NS: 183.33 , 90 , in comparison with thewas drastically decrease than that for the NS group 0.05). (B) The VGB six.8 two.62, fewer severeseizures typical saline group had p 0.05) (N = 7 in seizures for the VGB group (VGB: four.six 1.14; NS: (stage 3 3 and above), as in comparison to the NS group (VGB: 40 ; NS: 90 , p 0.05). (C) The imply count of daily seizures (stage and above), as compared to the NS group (VGB: 40 ; NS: 90 , p 0.05). (C) The mean count of everyday seizures for each and every group). the VGBVGB group was considerably decrease than that the NS group (VGB: 4.6 1.14; NS: six.86.8 2.62, p 0.05) (N = 7in for the group was drastically reduce than that for for the NS group (VGB: 4.six 1.14; NS: two.62, p 0.05) (N = 7 in every group). each and every group).3.2. The VGB-Treated Rats Had Much less Post-Status Epilepticus Chronic Hippocampal Damage3.two. The VGB-Treated Rats the cresyl Post-StatusEpilepticus Chronicthe VGB group had sigAfter VGB-Treated Rats Had Less violet staining showed that Hippocampal Harm three.two. The epileptogenesis, Had SigCD158a/KIR2DL1 Proteins custom synthesis nificantly less Post-Status Epilepticus Chronic Hippocampal Damage nificantly significantly less neuron loss within the hippocampal CA3 field (see Figure 3A)the VGB NS group Soon after epileptogenesis, the cresyl violet staining showed that thethan the group had Right after epileptogenesis, the cresyl violet staining showed that VGB group had sig(see Figure 3B).lessblind semi-quantitative evaluation showed that the VGB group had sigsignificantly A neuron lossthe the hippocampal CA3 field Figure 3A) than the NS group nificantly much less neuron loss in in hippocampal CA3 field (see (see Figure 3A) than the NS nificantly lessFigure 3B). A blind semi-quantitative evaluation showed that the VGB two.1 neuronal harm compared with (VGB: group group (see hippocampalsemi-quantitative evaluation showed the NS group group had sig(see Figure 3B). A blind that the VGB 0.three; NS: 2.9 0.4, p significantly less hippocampal 3C). In conclusion,compared together with the NS group (VGB: had drastically 0.01) (See Figure neuronal damage the VGB-treated group exhibited nificantly much less hippocampal neuronal damage compared together with the NS group (VGB: two.1 much less chronic NS: two.9 0.4, damage post-pilocarpine-induced status epilepticus. 2.1 0.three; hippocampal p 0.01) (See Figure 3C). In conclusion, the VGB-treated group 0.three; NS: two.9 0.four, p 0.01) (See Figure 3C). In conclusion, the VGB-treated group exhibited exhibited much less chronic hippocampal damage post-pilocarpine-induced status epilepticus. much less chronic hippocampal harm post-pilocarpine-induced status epilepticus.Figure three. VGB-treated rats had much less post-status epilepticus chronic hippocampal damage. The VGB Figure three. VGB-treated rats had much less post-status epilepticus chronic hippocampal harm. The VGB group (A) had considerably significantly less neuron loss within the hippocampal CA3 region than was the case in group (A) had significantly significantly less neuron loss within the hippocampal CA3 area than was the case inside the the NS three. VGB-treated rats had significantly less post-status staining). A chronic hipp.