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.