Monophosphoryl lipid A-induced delayed preconditioning is mediated by calcitonin gene-related peptide.

  title={Monophosphoryl lipid A-induced delayed preconditioning is mediated by calcitonin gene-related peptide.},
  author={Shajin He and Han-wu Deng and Y J Li},
  journal={European journal of pharmacology},
  volume={420 2-3},
  • S. HeH. DengY. Li
  • Published 25 May 2001
  • Biology, Chemistry
  • European journal of pharmacology

Delayed cardioprotection induced by nitroglycerin is mediated by alpha-calcitonin gene-related peptide

The present results suggest that the delayed cardioprotection induced by nitroglycerin is mediated mainly by the α-CGRP isoform via the NO-cGMP pathway.

Monophosphoryl Lipid A-Induced Delayed Preconditioning in Rat Small Intestine Is Mediated by Calcitonin Gene-Related Peptide

Monophosphoryl lipid A pharmacologically mimics delayed preconditioning and the protective effects are related to the stimulation of calcitonin gene-related peptide release in rat small intestine.

Pharmacological preconditioning with monophosphoryl lipid A improves post ischemic diastolic function and modifies TNF-alpha synthesis.

  • R. SharonyI. Frolkis G. Uretzky
  • Biology, Medicine
    European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery
  • 2005

Nitroglycerin Protects Small Intestine from Ischemia–Reperfusion Injury via NO–cGMP Pathway and Upregulation of α-CGRP

NTG prevents rat small intestine from I/R injury by delayed PCL effects 24 h after administration and its protective effects are mediated by NO–cGMP pathway and α-CGRP upregulation.



Early and delayed cardioprotection by heat stress is mediated by calcitonin gene-related peptide

The present study suggests that, in the rat, the early and delayed cardioprotection induced by heat stress involves endogenous CGRP.

Role of inducible nitric oxide synthase in pharmacological "preconditioning" with monophosphoryl lipid A.

It is suggested that MLA pretreatment may enhance iNOS enzyme activity by MLA during ischemia which may be responsible for the observed cardioprotection.

Preconditioning of rat heart with monophosphoryl lipid A: a role for nitric oxide.

It is demonstrated that MLA induced the expression of iNOS and protected the myocardium from ischemic reperfusion injury which is blocked by an inhibitor of NO synthesis, which suggests a role of NO in MLA-mediated cardioprotection.

Aggravation of myocardial infarction in the porcine heart by capsaicin-induced depletion of calcitonin gene-related peptide (CGRP).

This study indicates that peptides released from cardiac C fibers have a beneficial effect in myocardial ischemia and reperfusion and is a possible candidate for the mediation of the observed cardioprotective effect.

Essential role of inducible nitric oxide synthase in monophosphoryl lipid A-induced late cardioprotection: evidence from pharmacological inhibition and gene knockout mice.

An obligatory role for iNOS in mediating the cardioprotective effect induced by MLA was confirmed with the pharmacological inhibition and gene knockout mice, demonstrating a direct association of infarct size reduction with increased NO production with MLA350.

Preservation of global cardiac function in the rabbit following protracted ischemia/reperfusion using monophosphoryl lipid A (MLA).

Evaluating the ability of monophosphoryl lipid A to preserve global cardiac function and peripheral hemodynamics in a rabbit model of prolonged regional ischemia, reperfusion and evaluation of potential mechanisms by which MLA may preserve cardiac function suggest that a 24-h pretreatment with MLA was associated with preservation of global myocardial function.

Early and delayed protection by capsaicin against reperfusion injury in rat hearts.

  • F. ZhouY. LiH. Deng
  • Biology, Chemistry
    Zhongguo yao li xue bao = Acta pharmacologica Sinica
  • 1999
Pretreatment with capsaicin induces the early and delayed cardioprotection, which may be related to stimulation of CGRP release in the rat.