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Neuroprotective effect of calcitriol on ischemic/reperfusion injury through the NR3A/CREB pathways in the rat hippocampus.
Mol Med Rep. 2013 Dec; 8(6):1708-14.MM

Abstract

Calcitriol has been demonstrated to provide neuroprotection against ischemia/reperfusion (I/R) injury. However, the exact mechanism of this protection remains unknown. In the present study, the neuroprotective effect of calcitriol was investigated in rats exposed to cerebral I/R injury induced by middle cerebral artery occlusion (MCAO). In addition, the involvement of NR3A, extracellular signal‑regulated kinase 1/2 (ERK1/2), and phosphorylated cAMP/Ca2+‑response element binding protein (p‑CREB) in this protective action was determined in the hippocampal neurons. Western blot analysis was conducted to analyze the protein levels of NR3A, mitogen‑activated protein kinase kinase (MEK) and p‑CREB. The immunoreactivity of p‑CREB and NR3A were measured by quantum dot‑based immunofluorescence analysis. Results showed that MCAO rats exhibited large cortical infarct volumes. By contrast, intraperitoneal administration of calcitriol significantly reduced infarct volumes seven days following reperfusion, and these results were accompanied by elevated NR3A and p‑CREB activity in the hippocampal neurons. The inhibition of MEK by the addition of PD98059 led to attenuation of the neuroprotective effects of calcitriol and a correlated decrease in CREB activity. The results also demonstrated that calcitriol protected the brain from I/R injury through the NR3A‑MEK/ERK‑CREB pathway.

Authors+Show Affiliations

Department of Anesthesiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, P.R. China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

24141895

Citation

Fu, Jun, et al. "Neuroprotective Effect of Calcitriol On Ischemic/reperfusion Injury Through the NR3A/CREB Pathways in the Rat Hippocampus." Molecular Medicine Reports, vol. 8, no. 6, 2013, pp. 1708-14.
Fu J, Xue R, Gu J, et al. Neuroprotective effect of calcitriol on ischemic/reperfusion injury through the NR3A/CREB pathways in the rat hippocampus. Mol Med Rep. 2013;8(6):1708-14.
Fu, J., Xue, R., Gu, J., Xiao, Y., Zhong, H., Pan, X., & Ran, R. (2013). Neuroprotective effect of calcitriol on ischemic/reperfusion injury through the NR3A/CREB pathways in the rat hippocampus. Molecular Medicine Reports, 8(6), 1708-14. https://doi.org/10.3892/mmr.2013.1734
Fu J, et al. Neuroprotective Effect of Calcitriol On Ischemic/reperfusion Injury Through the NR3A/CREB Pathways in the Rat Hippocampus. Mol Med Rep. 2013;8(6):1708-14. PubMed PMID: 24141895.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroprotective effect of calcitriol on ischemic/reperfusion injury through the NR3A/CREB pathways in the rat hippocampus. AU - Fu,Jun, AU - Xue,Rui, AU - Gu,Junfeng, AU - Xiao,Yun, AU - Zhong,Heying, AU - Pan,Xuelian, AU - Ran,Ran, Y1 - 2013/10/14/ PY - 2013/03/25/received PY - 2013/09/23/accepted PY - 2013/10/22/entrez PY - 2013/10/22/pubmed PY - 2014/5/29/medline SP - 1708 EP - 14 JF - Molecular medicine reports JO - Mol Med Rep VL - 8 IS - 6 N2 - Calcitriol has been demonstrated to provide neuroprotection against ischemia/reperfusion (I/R) injury. However, the exact mechanism of this protection remains unknown. In the present study, the neuroprotective effect of calcitriol was investigated in rats exposed to cerebral I/R injury induced by middle cerebral artery occlusion (MCAO). In addition, the involvement of NR3A, extracellular signal‑regulated kinase 1/2 (ERK1/2), and phosphorylated cAMP/Ca2+‑response element binding protein (p‑CREB) in this protective action was determined in the hippocampal neurons. Western blot analysis was conducted to analyze the protein levels of NR3A, mitogen‑activated protein kinase kinase (MEK) and p‑CREB. The immunoreactivity of p‑CREB and NR3A were measured by quantum dot‑based immunofluorescence analysis. Results showed that MCAO rats exhibited large cortical infarct volumes. By contrast, intraperitoneal administration of calcitriol significantly reduced infarct volumes seven days following reperfusion, and these results were accompanied by elevated NR3A and p‑CREB activity in the hippocampal neurons. The inhibition of MEK by the addition of PD98059 led to attenuation of the neuroprotective effects of calcitriol and a correlated decrease in CREB activity. The results also demonstrated that calcitriol protected the brain from I/R injury through the NR3A‑MEK/ERK‑CREB pathway. SN - 1791-3004 UR - https://www.unboundmedicine.com/medline/citation/24141895/Neuroprotective_effect_of_calcitriol_on_ischemic/reperfusion_injury_through_the_NR3A/CREB_pathways_in_the_rat_hippocampus_ L2 - http://www.spandidos-publications.com/mmr/8/6/1708 DB - PRIME DP - Unbound Medicine ER -