# A Novel Postconditioning Approach Attenuates Myocardial Ischaemia-Reperfusion Injury in Rats

**Authors:** Lin Zhao, Yanghong Liu, Ye Chen, Zaixin Yu, Hui Luo

PMC · DOI: 10.31083/j.rcm2502067 · 2024-02-18

## TL;DR

A new method of postconditioning in rats reduces heart damage caused by restoring blood flow after a blockage.

## Contribution

A novel balloon-based postconditioning approach is introduced for rodents to study IRI.

## Key findings

- The balloon method allowed precise control of coronary blood flow during postconditioning.
- Postconditioning reduced infarct size and cardiac apoptosis in rats with IRI.
- Bcl-2 levels increased while Bax and cleaved caspase-3 levels decreased after postconditioning.

## Abstract

Ischaemia-reperfusion injury (IRI) is the damage that 
occurs when blood flow is restored to a tissue or organ after a period of 
ischaemia. Postconditioning is a therapeutic strategy aimed at reducing the 
tissue damage caused by IRI. Postconditioning in rodents is a useful tool to 
investigate the potential mechanisms of postconditioning. Currently, there is no 
convenient approach for postconditioning rodents.

Rats were 
subjected to a balloon postconditioning procedure. A balloon was used to control 
the flow in the vessel. This allowed for easy and precise manipulation of 
perfusion. Evans blue and triphenyltetrazolium chloride (TTC) double staining 
were used to determine the infarct size. Apoptosis in the myocardium was 
visualised and quantified by terminal deoxynucleotidyl transferase dUTP nick end 
labeling (TUNEL). Western blotting was performed to assess the expression of key 
apoptotic proteins, i.e., B-cell lymphoma 2 (Bcl-2), Bcl-2 Associated X 
(Bax), and cleaved caspase-3.

The balloon control approach to 
postconditioning provided accurate control of coronary blood flow and simplified 
the postconditioning manipulation. Infarct size reduction was observed in IRI 
rats after post-conditioning. There was a decrease in cardiac apoptosis in IRI 
rats after conditioning, as detected by TUNEL staining. IRI rats showed increased 
Bcl-2 levels and decreased Bax and cleaved caspase-3 levels in the myocardium.

Postconditioning was successfully applied in rats using 
this novel approach. Postconditioning with this approach reduced infarct size and 
apoptosis in the area at risk.

## Linked entities

- **Species:** Rattus norvegicus (taxon 10116)

## Full-text entities

- **Genes:** CASP3 (caspase 3) [NCBI Gene 836] {aka CPP32, CPP32B, SCA-1}, BCL2 (BCL2 apoptosis regulator) [NCBI Gene 596] {aka Bcl-2, PPP1R50}, BAX (BCL2 associated X, apoptosis regulator) [NCBI Gene 581] {aka BCL2L4}
- **Diseases:** ischaemia (MESH:D007511), cardiac apoptosis (MESH:D006331), Infarct size (MESH:D007238), damage (MESH:D020263), Myocardial Ischaemia-Reperfusion Injury (MESH:D015428), IRI (MESH:D015427)
- **Chemicals:** TTC (MESH:C009591), Evans blue (MESH:D005070), dUTP (MESH:C027078)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11263150/full.md

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Source: https://tomesphere.com/paper/PMC11263150