Figure 1.
Lithium treatment reduced HI brain injury.
A. The study design. B. Representative MAP2 staining from the dorsal hippocampus (left panels) and striatum (right panels) 12 weeks post-HI in vehicle-treated (upper panels) and lithium-treated rats (lower panels). C. The total volume of tissue loss 12 weeks after HI was reduced by 38.8% in lithium-treated mice (n = 23) compared with vehicle-treated mice (n = 21). D. The total pathological score. E. Neuropathological scores revealed less injury in the observed brain regions (except the hippocampus) after lithium treatment. Cx = cortex, Hip = hippocampus, Str = striatum, and Tha = thalamus; *p<0.05, **p<0.01.
Figure 2.
Accumulated distance moved. The HI rats treated with vehicle moved a longer distance during the 20 min analysis period (n = 13 for vehicle and n = 15 for lithium treated non-HI groups. n = 21 for vehicle and n = 23 for lithium treated HI groups). *p<0.05, **p<0.01.
Figure 3.
Neurogenesis in the dentate gyrus.
A. Representative DCX staining in the contralateral dentate gyrus 12 weeks post-HI in vehicle-treated (upper panel) and lithium-treated (lower panel) rats, reflecting hippocampal neurogenesis. B. The number of DCX-positive cells was not significantly different between vehicle- and lithium-treated control groups (n = 13 for vehicle and n = 15 for lithium treated groups). The number of DCX-positive cells increased after the insult and was 21.3% higher in the lithium-treated group than in the vehicle-treated group (n = 21 for vehicle n = 13 for lithium treated group). **p<0.001.
Figure 4.
Serum cytokines and microglia activation.
A. The serum levels of IL-1α, IL-1β, and IL-6 were increased after HI, and lithium treatment normalized these levels (n = 5/group). B. Representative Iba-1 immunostaining in the cortex of a normal control rat (left panel), an HI-exposed rat after vehicle treatment (middle panel), and an HI-exposed rat after lithium treatment (right panel) 12 weeks after HI. C. Representative galectin-3 staining in the border zone of the cortex 12 weeks after HI. D. Double labeling of Iba1 (red) and galectin-3 (green) in the border zone of the cortex 12 weeks after HI demonstrating that very few Iba1-positive cells were also galectin-3-positive. E. Morphology of Iba1-positive cells indicating ramified (surveillance microglia), hyper-ramified (intermediate) microglia, and un-ramified (bushy or amoeboid) microglia. F. Percentage of Iba1-positive cells according to morphology in the border zone of the cortical injury after HI (n = 10/group). Scale bar = 20 µm. *p<0.05.
Figure 5.
A. HI rats had a slightly slower body weight gain during weeks 6 to 8 after birth. Lithium treatment had no effect on body weight gain, neither in control rats nor after HI. B. The brain weight was lower after HI compared to the non-HI controls. The weights of the kidneys and spleens were not significantly different among the groups (n = 13 for vehicle and n = 15 for lithium treated non-HI groups. n = 21 for vehicle and n = 23 for lithium treated HI groups). **p<0.01, ***p<0.001.