Linarin could protect myocardial tissue from the injury of Ischemia-reperfusion through activating Nrf-2.

Abstract

OBJECTIVES:

As we all know, oxidative stress was one of the most important causes of ischemia-reperfusion injury. And it was reported that Nrf-2 as an important regulator for oxidative stress could be activated by Linarin. Thus it would be interesting to find whether Linarin could inhibit ischemia-reperfusion injury through activating Nrf-2.

METHODS:

In this study, cell activity was detected by MTT assay and caspase-3 activity detection kit. And the expressions or activities of some signal proteins were evaluated by western-blot or activity detection kits. At last, the effect and mechanism of Linarin on heart tissues were verified in the ischemia-reperfusion model of isolated hearts.

RESULTS:

The proliferation activity of cell was inhibited while the apoptosis rate was increased after hypoxia-reoxygenation. However, Linarin could inhibit these two variations. It was found that these effects of Linarin were related with the activation of Nrf-2 through PI3K/Akt signaling pathway. Meanwhile, the anti-oxidative enzymes, regulated by Nrf-2, were enhanced to against the oxidative stress caused by hypoxia-reoxygenation. And with the inhibition of oxidative stress, some proliferation and apoptosis related proteins such as NF-kB and Cytochrome C were adjusted to support the viability of cells. At last, these results were verified in the ischemia reperfusion experiment of isolated hearts.

CONCLUSIONS:

From this study, we assured that LIN could protect myocardial tissue from ischemia-reperfusion through activating Nrf-2.

• Authors: Qian Yu, Xin Li, Xia Cao
• Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie (Biomed Pharmacother) Vol. 90 Pg. 1-7 (Jun 2017) ISSN: 1950-6007 [Electronic] France
• PMID: 28340376 (Publication Type: Journal Article)
• Copyright: Copyright © 2017 Elsevier Masson SAS. All rights reserved.

Chemical References

• Antioxidants
• Glycosides
• NF-E2-Related Factor 2
• NF-kappa B
• Protective Agents
• Cytochromes c
• Phosphatidylinositol 3-Kinases
• linarin

Topics

• Animals
• Antioxidants (metabolism)
• Apoptosis (drug effects)
• Cell Line
• Cytochromes c (metabolism)
• Glycosides (pharmacology)
• Heart (drug effects)
• Myocardial Reperfusion Injury (drug therapy, metabolism)
• Myocardium (metabolism)
• NF-E2-Related Factor 2 (metabolism)
• NF-kappa B (metabolism)
• Oxidative Stress (drug effects)
• Phosphatidylinositol 3-Kinases (metabolism)
• Protective Agents (pharmacology)
• Rats
• Signal Transduction (drug effects)