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Prophylactic Subacute Administration of Zinc Increases CCL2, CCR2, FGF2, and IGF-1 Expression and Prevents the Long-Term Memory Loss in a Rat Model of Cerebral Hypoxia-Ischemia.

Blanco-Alvarez VM, Soto-Rodriguez G, Gonzalez-Barrios JA, Martinez-Fong D, Brambila E, Torres-Soto M, Aguilar-Peralta AK, Gonzalez-Vazquez A, Tomás-Sanchez C, Limón ID, Eguibar JR, Ugarte A, Hernandez-Castillo J, Leon-Chavez BA - Neural Plast. (2015)

Bottom Line: Chemokines and growth factors are also involved in the neuroprotective effect in hypoxia-ischemia.Subacute administration of zinc increased expression of CCL2, CCR2, FGF2, and IGF-1 in the early and late phases of postreperfusion and prevented the CCAO-induced memory loss in the rat.These results might be explained by the induction of neural plasticity because of the expression of CCL2 and growth factors.

View Article: PubMed Central - PubMed

Affiliation: Facultad de Ciencias Químicas, BUAP, 14 Sur y Avenida San Claudio, 72570 Puebla, PUE, Mexico.

ABSTRACT
Prophylactic subacute administration of zinc decreases lipoperoxidation and cell death following a transient cerebral hypoxia-ischemia, thus suggesting neuroprotective and preconditioning effects. Chemokines and growth factors are also involved in the neuroprotective effect in hypoxia-ischemia. We explored whether zinc prevents the cerebral cortex-hippocampus injury through regulation of CCL2, CCR2, FGF2, and IGF-1 expression following a 10 min of common carotid artery occlusion (CCAO). Male rats were grouped as follows: (1) Zn96h, rats injected with ZnCl2 (one dose every 24 h during four days); (2) Zn96h + CCAO, rats treated with ZnCl2 before CCAO; (3) CCAO, rats with CCAO only; (4) Sham group, rats with mock CCAO; and (5) untreated rats. The cerebral cortex-hippocampus was dissected at different times before and after CCAO. CCL2/CCR2, FGF2, and IGF-1 expression was assessed by RT-PCR and ELISA. Learning in Morris Water Maze was achieved by daily training during 5 days. Long-term memory was evaluated on day 7 after learning. Subacute administration of zinc increased expression of CCL2, CCR2, FGF2, and IGF-1 in the early and late phases of postreperfusion and prevented the CCAO-induced memory loss in the rat. These results might be explained by the induction of neural plasticity because of the expression of CCL2 and growth factors.

No MeSH data available.


Related in: MedlinePlus

Effect of subacute administration of zinc on CCL2 expression in cerebral cortex-hippocampus of the rat. RT-PCR was used to determine mRNA levels of CCL2 (323 bp) and GA3PDH (420 bp). ((a) and (b)) Showing representative photographs of ethidium-bromide-stained RT-PCR products fractionated on 2% agarose gel and the respective densitometry analysis. ((c) and (d)) Showing the CCL2 protein levels using ELISA. Each value represents the mean ± SEM of 5 independent experiments made in triplicate. (1) Zn96h, rats injected with ZnCl2 (one dose every 24 h during 4 days). (2) Zn96h + CCAO, rats treated with zinc before 10 min of common carotid artery occlusion (CCAO). (3) CCAO, rats with CCAO only. (4) Sham group, rats with mock CCAO. (5) Untreated rats. ∗, significant when compared with the control group; ANOVA test and post hoc Dunnett's test. †, significant when compared between groups; unpaired Student's t-test. P < 0.05.
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fig1: Effect of subacute administration of zinc on CCL2 expression in cerebral cortex-hippocampus of the rat. RT-PCR was used to determine mRNA levels of CCL2 (323 bp) and GA3PDH (420 bp). ((a) and (b)) Showing representative photographs of ethidium-bromide-stained RT-PCR products fractionated on 2% agarose gel and the respective densitometry analysis. ((c) and (d)) Showing the CCL2 protein levels using ELISA. Each value represents the mean ± SEM of 5 independent experiments made in triplicate. (1) Zn96h, rats injected with ZnCl2 (one dose every 24 h during 4 days). (2) Zn96h + CCAO, rats treated with zinc before 10 min of common carotid artery occlusion (CCAO). (3) CCAO, rats with CCAO only. (4) Sham group, rats with mock CCAO. (5) Untreated rats. ∗, significant when compared with the control group; ANOVA test and post hoc Dunnett's test. †, significant when compared between groups; unpaired Student's t-test. P < 0.05.

Mentions: Protein and mRNA levels of CCL2, CCR2, FGF2, and IGF-1 were determined in the cerebral cortex-hippocampus to find out whether a subacute administration of zinc causes a preconditioning effect in CCAO model. Our results showed that 10 min CCAO did not modify the levels of CCL2 mRNA (Figure 1(a)) and protein (Figure 1(c)) after reperfusion when compared with the untreated control (time 0). A statistically significant difference was observed when mRNA values in the CCAO group were compared with the sham group at 12 h, 24 h, 36 h, and 168 h (Figure 1(a)) and for protein at 96 h (Figure 1(c)). The subacute administration of zinc produced upregulation of CCL2 mRNA by 169%  ±  17% at 48 h and 178%  ±  73% at 24 h before time 0 and by 151%  ±  4% at 96 h after time 0 (Figure 1(b)). After CCAO, no change in the level of CCL2 was observed in rats treated with zinc (Figure 1(b)). The CCL2 protein levels increased by 146%  ±  27% at time 0 and by 64%  ±  12% at 12 h after reperfusion in rats treated with zinc (Figure 1(d)).


Prophylactic Subacute Administration of Zinc Increases CCL2, CCR2, FGF2, and IGF-1 Expression and Prevents the Long-Term Memory Loss in a Rat Model of Cerebral Hypoxia-Ischemia.

Blanco-Alvarez VM, Soto-Rodriguez G, Gonzalez-Barrios JA, Martinez-Fong D, Brambila E, Torres-Soto M, Aguilar-Peralta AK, Gonzalez-Vazquez A, Tomás-Sanchez C, Limón ID, Eguibar JR, Ugarte A, Hernandez-Castillo J, Leon-Chavez BA - Neural Plast. (2015)

Effect of subacute administration of zinc on CCL2 expression in cerebral cortex-hippocampus of the rat. RT-PCR was used to determine mRNA levels of CCL2 (323 bp) and GA3PDH (420 bp). ((a) and (b)) Showing representative photographs of ethidium-bromide-stained RT-PCR products fractionated on 2% agarose gel and the respective densitometry analysis. ((c) and (d)) Showing the CCL2 protein levels using ELISA. Each value represents the mean ± SEM of 5 independent experiments made in triplicate. (1) Zn96h, rats injected with ZnCl2 (one dose every 24 h during 4 days). (2) Zn96h + CCAO, rats treated with zinc before 10 min of common carotid artery occlusion (CCAO). (3) CCAO, rats with CCAO only. (4) Sham group, rats with mock CCAO. (5) Untreated rats. ∗, significant when compared with the control group; ANOVA test and post hoc Dunnett's test. †, significant when compared between groups; unpaired Student's t-test. P < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig1: Effect of subacute administration of zinc on CCL2 expression in cerebral cortex-hippocampus of the rat. RT-PCR was used to determine mRNA levels of CCL2 (323 bp) and GA3PDH (420 bp). ((a) and (b)) Showing representative photographs of ethidium-bromide-stained RT-PCR products fractionated on 2% agarose gel and the respective densitometry analysis. ((c) and (d)) Showing the CCL2 protein levels using ELISA. Each value represents the mean ± SEM of 5 independent experiments made in triplicate. (1) Zn96h, rats injected with ZnCl2 (one dose every 24 h during 4 days). (2) Zn96h + CCAO, rats treated with zinc before 10 min of common carotid artery occlusion (CCAO). (3) CCAO, rats with CCAO only. (4) Sham group, rats with mock CCAO. (5) Untreated rats. ∗, significant when compared with the control group; ANOVA test and post hoc Dunnett's test. †, significant when compared between groups; unpaired Student's t-test. P < 0.05.
Mentions: Protein and mRNA levels of CCL2, CCR2, FGF2, and IGF-1 were determined in the cerebral cortex-hippocampus to find out whether a subacute administration of zinc causes a preconditioning effect in CCAO model. Our results showed that 10 min CCAO did not modify the levels of CCL2 mRNA (Figure 1(a)) and protein (Figure 1(c)) after reperfusion when compared with the untreated control (time 0). A statistically significant difference was observed when mRNA values in the CCAO group were compared with the sham group at 12 h, 24 h, 36 h, and 168 h (Figure 1(a)) and for protein at 96 h (Figure 1(c)). The subacute administration of zinc produced upregulation of CCL2 mRNA by 169%  ±  17% at 48 h and 178%  ±  73% at 24 h before time 0 and by 151%  ±  4% at 96 h after time 0 (Figure 1(b)). After CCAO, no change in the level of CCL2 was observed in rats treated with zinc (Figure 1(b)). The CCL2 protein levels increased by 146%  ±  27% at time 0 and by 64%  ±  12% at 12 h after reperfusion in rats treated with zinc (Figure 1(d)).

Bottom Line: Chemokines and growth factors are also involved in the neuroprotective effect in hypoxia-ischemia.Subacute administration of zinc increased expression of CCL2, CCR2, FGF2, and IGF-1 in the early and late phases of postreperfusion and prevented the CCAO-induced memory loss in the rat.These results might be explained by the induction of neural plasticity because of the expression of CCL2 and growth factors.

View Article: PubMed Central - PubMed

Affiliation: Facultad de Ciencias Químicas, BUAP, 14 Sur y Avenida San Claudio, 72570 Puebla, PUE, Mexico.

ABSTRACT
Prophylactic subacute administration of zinc decreases lipoperoxidation and cell death following a transient cerebral hypoxia-ischemia, thus suggesting neuroprotective and preconditioning effects. Chemokines and growth factors are also involved in the neuroprotective effect in hypoxia-ischemia. We explored whether zinc prevents the cerebral cortex-hippocampus injury through regulation of CCL2, CCR2, FGF2, and IGF-1 expression following a 10 min of common carotid artery occlusion (CCAO). Male rats were grouped as follows: (1) Zn96h, rats injected with ZnCl2 (one dose every 24 h during four days); (2) Zn96h + CCAO, rats treated with ZnCl2 before CCAO; (3) CCAO, rats with CCAO only; (4) Sham group, rats with mock CCAO; and (5) untreated rats. The cerebral cortex-hippocampus was dissected at different times before and after CCAO. CCL2/CCR2, FGF2, and IGF-1 expression was assessed by RT-PCR and ELISA. Learning in Morris Water Maze was achieved by daily training during 5 days. Long-term memory was evaluated on day 7 after learning. Subacute administration of zinc increased expression of CCL2, CCR2, FGF2, and IGF-1 in the early and late phases of postreperfusion and prevented the CCAO-induced memory loss in the rat. These results might be explained by the induction of neural plasticity because of the expression of CCL2 and growth factors.

No MeSH data available.


Related in: MedlinePlus