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Investigating the involvement of glycogen synthase kinase-3β and gap junction signaling in TRPV1 and remote hind preconditioning-induced cardioprotection.
Eur J Pharmacol. 2017 Nov 05; 814:9-17.EJ

Abstract

Remote ischemic preconditioning (RIPC) is the phenomenon that harnesses the body's endogenous protective mechanisms against prolonged ischemia-reperfusion-induced injury. The present study aimed to explore the involvement of glycogen synthase kinase-3β and gap junction signaling in TRPV1 and remote hind preconditioning-induced cardioprotection. In the present study, four consecutive cycles (5min of ischemia-reperfusion) of remote hind limb preconditioning stimulus were delivered using a blood pressure cuff fastened at the inguinal level of the rat. The isolated rat hearts were mounted on the Langendorff's apparatus and were exposed to 30min of global ischemia-120min of reperfusion. Sustained ischemia-reperfusion led to cardiac injury that was assessed in terms of infarct size, LDH release, CK release, LVDP, +dp/dtmax, -dp/dtmin, heart rate and coronary flow rate. The pharmacological agents employed in the present study included capsaicin (10mg/kg) as TRPV1 channel activator, AR-A014418 (1 and 3mg/kg) as glycogen synthase kinase-3β inhibitor and carbenoxolone disodium (50 and 100mg/kg) as gap junction blocker. Remote hind limb, capsaicin and AR-A014418 preconditioning led to significant reduction in the infarct size, LDH release, CK release and improved LVDP, +dp/dtmax, -dp/dtmin, heart rate and coronary flow rate. However, remote hind limb, capsaicin and AR-A014418 preconditioning-induced cardioprotective effects were remarkably reduced in the presence of carbenoxolone (100mg/kg). This indicates that remote preconditioning stimulus probably activates TRPV1 channels that may inhibit glycogen synthase kinase-3β activity which subsequently enhances gap junction coupling to produce cardioprotective effects.

Authors+Show Affiliations

Department of Pharmaceutical Sciences and Drug Research, Punjabi University Patiala, 147002 India.Department of Pharmaceutical Sciences and Drug Research, Punjabi University Patiala, 147002 India. Electronic address: amteshwarjaggi@yahoo.co.in.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28755986

Citation

Randhawa, Puneet Kaur, and Amteshwar Singh Jaggi. "Investigating the Involvement of Glycogen Synthase Kinase-3β and Gap Junction Signaling in TRPV1 and Remote Hind Preconditioning-induced Cardioprotection." European Journal of Pharmacology, vol. 814, 2017, pp. 9-17.
Randhawa PK, Jaggi AS. Investigating the involvement of glycogen synthase kinase-3β and gap junction signaling in TRPV1 and remote hind preconditioning-induced cardioprotection. Eur J Pharmacol. 2017;814:9-17.
Randhawa, P. K., & Jaggi, A. S. (2017). Investigating the involvement of glycogen synthase kinase-3β and gap junction signaling in TRPV1 and remote hind preconditioning-induced cardioprotection. European Journal of Pharmacology, 814, 9-17. https://doi.org/10.1016/j.ejphar.2017.07.045
Randhawa PK, Jaggi AS. Investigating the Involvement of Glycogen Synthase Kinase-3β and Gap Junction Signaling in TRPV1 and Remote Hind Preconditioning-induced Cardioprotection. Eur J Pharmacol. 2017 Nov 5;814:9-17. PubMed PMID: 28755986.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Investigating the involvement of glycogen synthase kinase-3β and gap junction signaling in TRPV1 and remote hind preconditioning-induced cardioprotection. AU - Randhawa,Puneet Kaur, AU - Jaggi,Amteshwar Singh, Y1 - 2017/07/27/ PY - 2017/05/15/received PY - 2017/07/26/revised PY - 2017/07/26/accepted PY - 2017/8/2/pubmed PY - 2018/6/2/medline PY - 2017/7/31/entrez KW - Gap junction KW - Glycogen synthase kinase-3β KW - Heart KW - Remote preconditioning KW - TRPV SP - 9 EP - 17 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 814 N2 - Remote ischemic preconditioning (RIPC) is the phenomenon that harnesses the body's endogenous protective mechanisms against prolonged ischemia-reperfusion-induced injury. The present study aimed to explore the involvement of glycogen synthase kinase-3β and gap junction signaling in TRPV1 and remote hind preconditioning-induced cardioprotection. In the present study, four consecutive cycles (5min of ischemia-reperfusion) of remote hind limb preconditioning stimulus were delivered using a blood pressure cuff fastened at the inguinal level of the rat. The isolated rat hearts were mounted on the Langendorff's apparatus and were exposed to 30min of global ischemia-120min of reperfusion. Sustained ischemia-reperfusion led to cardiac injury that was assessed in terms of infarct size, LDH release, CK release, LVDP, +dp/dtmax, -dp/dtmin, heart rate and coronary flow rate. The pharmacological agents employed in the present study included capsaicin (10mg/kg) as TRPV1 channel activator, AR-A014418 (1 and 3mg/kg) as glycogen synthase kinase-3β inhibitor and carbenoxolone disodium (50 and 100mg/kg) as gap junction blocker. Remote hind limb, capsaicin and AR-A014418 preconditioning led to significant reduction in the infarct size, LDH release, CK release and improved LVDP, +dp/dtmax, -dp/dtmin, heart rate and coronary flow rate. However, remote hind limb, capsaicin and AR-A014418 preconditioning-induced cardioprotective effects were remarkably reduced in the presence of carbenoxolone (100mg/kg). This indicates that remote preconditioning stimulus probably activates TRPV1 channels that may inhibit glycogen synthase kinase-3β activity which subsequently enhances gap junction coupling to produce cardioprotective effects. SN - 1879-0712 UR - https://www.unboundmedicine.com/medline/citation/28755986/Investigating_the_involvement_of_glycogen_synthase_kinase_3β_and_gap_junction_signaling_in_TRPV1_and_remote_hind_preconditioning_induced_cardioprotection_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(17)30500-9 DB - PRIME DP - Unbound Medicine ER -