What is the clinical evidence from this study?

Population: Myocardial ischemia/reperfusion injury. Intervention: N-n-butyl haloperidol iodide (F2). Primary outcome: Egr-1 expression, hemodynamic parameters, MPO, cTnI, and TNF-alpha.

January 1, 2007Cellular Physiology and Biochemistry

The Protective Effects of N-n-butyl Haloperidol Iodide on Myocardial Ischemia-Reperfusion Injury in Rats by Inhibiting Egr-1 Overexpression

Q: What does this research mean for the field?

N-n-butyl haloperidol iodide protects myocardial tissues and cells from ischemia/reperfusion injury by inhibiting Egr-1 overexpression. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

View Full Paper

Ask AI

Bookmark

Key result

N-n-butyl haloperidol iodide protects rat myocardium from ischemia/reperfusion injury by inhibiting Egr-1 overexpression.

Population

Sprague-Dawley rat myocardial ischemia/reperfusion model and cardiomyocyte hypoxia/reoxygenation model

Design

Preclinical

Authors

YZYanmei ZhangChinese Academy of Tropical Agricultural Sciences GSGanggang ShiSecond Hospital of Tianjin Medical University JZJinhong ZhengShantou University

Discussion

Member takes

Implication

Hypothesis-generating for Egr-1 inhibition in myocardial protection; leaves open clinical translation pending human data.

Structured PICO

Population

Sprague-Dawley rat myocardial ischemia/reperfusion model and cardiomyocyte hypoxia/reoxygenation model.

Intervention

N-n-butyl haloperidol iodide (F2) and antisense Egr-1 oligodeoxyribonucleotide (ODN)

Outcome

Egr-1 mRNA and protein expression, hemodynamic parameters, myeloperoxidase (MPO), cardiac troponin I (cTnI), and tumor necrosis factor-alpha (TNF-alpha)surrogate

N-n-butyl haloperidol iodide protects against myocardial ischemia-reperfusion injury in rat models by inhibiting Egr-1 overexpression.

Cite This Study

Zhang et al. (2007) studied Myocardial ischemia/reperfusion injury. N-n-butyl haloperidol iodide (F2) was evaluated on Egr-1 expression, hemodynamic parameters, MPO, cTnI, and TNF-alpha. N-n-butyl haloperidol iodide (F2) protected rat myocardial tissues and cells from ischemia/reperfusion injury by inhibiting Egr-1 overexpression.

synapsesocial.com/papers/6aa7c7db0b3c98ee51310b4f https://doi.org/10.1159/000107547

View Full Paper

Ask AI

Bookmark

The Protective Effects of N-n-butyl Haloperidol Iodide on Myocardial Ischemia-Reperfusion Injury in Rats by Inhibiting Egr-1 Overexpression

Discussion

Member takes

Implication

Structured PICO

Cite This Study

The Protective Effects of N-n-butyl Haloperidol Iodide on Myocardial Ischemia-Reperfusion Injury in Rats by Inhibiting Egr-1 Overexpression

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider