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Diabetes abolishes the cardioprotection induced by sevoflurane postconditioning in the rat heart in vivo: roles of glycogen synthase kinase-3β and its upstream pathways.
J Surg Res. 2012 Nov; 178(1):96-104.JS

Abstract

BACKGROUND

We measured the cardioprotection afforded by sevoflurane postconditioning in streptozotocin-induced diabetic rats (DRs) and determined the roles of glycogen synthase kinase (GSK), phosphatidylinositol-3-kinase/Akt, and extracellular signal-regulated kinase (ERK1/2) in such a procedure.

METHODS

DRs and nondiabetic rats (NDRs) were subjected to a 30-min coronary artery occlusion followed by a 120-min reperfusion. Postconditioning was achieved by inhalation of 1 minimum alveolar concentration sevoflurane at the first 5 min of reperfusion. The infarct size was determined by triphenyltetrazolium chloride staining. Expressions of GSK-3β, Akt, and ERK1/2 were measured using Western blotting.

RESULTS

In NDRs, the infarct size was significantly decreased from 53.4% ± 7.6% to 34.9% ± 5.6% by sevoflurane postconditioning (P < 0.01). Such an anti-infarct effect was abolished completely in the DRs, as evidenced by a similar infarct size observed between the sevoflurane-treated and untreated DRs (49.3% ± 8.6% and 49.6% ± 9.3%, respectively, P > 0.05). Direct inhibition of GSK-3β by injection of SB216763 just before the start of reperfusion induced equivalent infarct-sparing effects in both NDRs (37.8% ± 3.9% and 53.4% ± 7.6% in SB216763-treated and untreated NDRs, respectively; P < 0.01) and DRs (38.8% ± 3.2% and 49.3% ± 8.6% in SB216763-treated and untreated DRs, respectively; P < 0.05). Sevoflurane postconditioning remarkably enhanced the phosphorylation of GSK-3β Ser(9), Akt Ser(473), and ERK1/2 in NDRs, which were blocked in DRs.

CONCLUSIONS

The cardioprotection induced by sevoflurane postconditioning is abolished by diabetes. This might be due to the impairment of phosphorylation of GSK-3β and its upstream signaling pathways of phosphatidylinositol-3-kinase/Akt and ERK1/2 in the presence of diabetes.

Authors+Show Affiliations

Department of Anesthesiology, First Affiliated Hospital, China Medical University, Liaoning, People's Republic of China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22482760

Citation

Tai, Wenjun, et al. "Diabetes Abolishes the Cardioprotection Induced By Sevoflurane Postconditioning in the Rat Heart in Vivo: Roles of Glycogen Synthase Kinase-3β and Its Upstream Pathways." The Journal of Surgical Research, vol. 178, no. 1, 2012, pp. 96-104.
Tai W, Shi E, Yan L, et al. Diabetes abolishes the cardioprotection induced by sevoflurane postconditioning in the rat heart in vivo: roles of glycogen synthase kinase-3β and its upstream pathways. J Surg Res. 2012;178(1):96-104.
Tai, W., Shi, E., Yan, L., Jiang, X., Ma, H., & Ai, C. (2012). Diabetes abolishes the cardioprotection induced by sevoflurane postconditioning in the rat heart in vivo: roles of glycogen synthase kinase-3β and its upstream pathways. The Journal of Surgical Research, 178(1), 96-104. https://doi.org/10.1016/j.jss.2012.02.021
Tai W, et al. Diabetes Abolishes the Cardioprotection Induced By Sevoflurane Postconditioning in the Rat Heart in Vivo: Roles of Glycogen Synthase Kinase-3β and Its Upstream Pathways. J Surg Res. 2012;178(1):96-104. PubMed PMID: 22482760.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Diabetes abolishes the cardioprotection induced by sevoflurane postconditioning in the rat heart in vivo: roles of glycogen synthase kinase-3β and its upstream pathways. AU - Tai,Wenjun, AU - Shi,Enyi, AU - Yan,Lihui, AU - Jiang,Xiaojing, AU - Ma,Hong, AU - Ai,Chunyu, Y1 - 2012/03/30/ PY - 2011/12/22/received PY - 2012/01/29/revised PY - 2012/02/09/accepted PY - 2012/4/10/entrez PY - 2012/4/10/pubmed PY - 2013/1/11/medline SP - 96 EP - 104 JF - The Journal of surgical research JO - J Surg Res VL - 178 IS - 1 N2 - BACKGROUND: We measured the cardioprotection afforded by sevoflurane postconditioning in streptozotocin-induced diabetic rats (DRs) and determined the roles of glycogen synthase kinase (GSK), phosphatidylinositol-3-kinase/Akt, and extracellular signal-regulated kinase (ERK1/2) in such a procedure. METHODS: DRs and nondiabetic rats (NDRs) were subjected to a 30-min coronary artery occlusion followed by a 120-min reperfusion. Postconditioning was achieved by inhalation of 1 minimum alveolar concentration sevoflurane at the first 5 min of reperfusion. The infarct size was determined by triphenyltetrazolium chloride staining. Expressions of GSK-3β, Akt, and ERK1/2 were measured using Western blotting. RESULTS: In NDRs, the infarct size was significantly decreased from 53.4% ± 7.6% to 34.9% ± 5.6% by sevoflurane postconditioning (P < 0.01). Such an anti-infarct effect was abolished completely in the DRs, as evidenced by a similar infarct size observed between the sevoflurane-treated and untreated DRs (49.3% ± 8.6% and 49.6% ± 9.3%, respectively, P > 0.05). Direct inhibition of GSK-3β by injection of SB216763 just before the start of reperfusion induced equivalent infarct-sparing effects in both NDRs (37.8% ± 3.9% and 53.4% ± 7.6% in SB216763-treated and untreated NDRs, respectively; P < 0.01) and DRs (38.8% ± 3.2% and 49.3% ± 8.6% in SB216763-treated and untreated DRs, respectively; P < 0.05). Sevoflurane postconditioning remarkably enhanced the phosphorylation of GSK-3β Ser(9), Akt Ser(473), and ERK1/2 in NDRs, which were blocked in DRs. CONCLUSIONS: The cardioprotection induced by sevoflurane postconditioning is abolished by diabetes. This might be due to the impairment of phosphorylation of GSK-3β and its upstream signaling pathways of phosphatidylinositol-3-kinase/Akt and ERK1/2 in the presence of diabetes. SN - 1095-8673 UR - https://www.unboundmedicine.com/medline/citation/22482760/Diabetes_abolishes_the_cardioprotection_induced_by_sevoflurane_postconditioning_in_the_rat_heart_in_vivo:_roles_of_glycogen_synthase_kinase_3β_and_its_upstream_pathways_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-4804(12)00092-3 DB - PRIME DP - Unbound Medicine ER -