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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

The subacute administration effect of zinc on FGF2 expression levels after hypoxia-ischemia in the rat. RT-PCR was used to determine mRNA levels of FGF2 (260 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 FGF2 protein levels measured 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 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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fig5: The subacute administration effect of zinc on FGF2 expression levels after hypoxia-ischemia in the rat. RT-PCR was used to determine mRNA levels of FGF2 (260 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 FGF2 protein levels measured 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 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: RT-PCR and ELISA were used to identify whether the subacute administration of zinc modifies the expression of FGF2 (Figure 5) and IGF1 (Figure 6) after CCAO. An increase in FGF2 mRNA levels by 40 ± 9% at 12 h and by 37 ± 6% at 96 h was detected after reperfusion (Figure 5(a)). The subacute administration of zinc caused a further increase in FGF2 mRNA by 214 ± 55% at 4 h, 141 ± 42% at 8 h, 149 ± 35% at 24 h, and 75 ± 9% at 36 h after reperfusion (Figure 5(b)).


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)

The subacute administration effect of zinc on FGF2 expression levels after hypoxia-ischemia in the rat. RT-PCR was used to determine mRNA levels of FGF2 (260 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 FGF2 protein levels measured 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 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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getmorefigures.php?uid=PMC4556331&req=5

fig5: The subacute administration effect of zinc on FGF2 expression levels after hypoxia-ischemia in the rat. RT-PCR was used to determine mRNA levels of FGF2 (260 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 FGF2 protein levels measured 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 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: RT-PCR and ELISA were used to identify whether the subacute administration of zinc modifies the expression of FGF2 (Figure 5) and IGF1 (Figure 6) after CCAO. An increase in FGF2 mRNA levels by 40 ± 9% at 12 h and by 37 ± 6% at 96 h was detected after reperfusion (Figure 5(a)). The subacute administration of zinc caused a further increase in FGF2 mRNA by 214 ± 55% at 4 h, 141 ± 42% at 8 h, 149 ± 35% at 24 h, and 75 ± 9% at 36 h after reperfusion (Figure 5(b)).

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