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Myocardial ischemia reperfusion injury (MIRI) is a complex pathophysiological process involved with the activation of oxidative stress, inflammation and apoptosis. Sappanone A (SA), a homoisoflavanone isolated from the heartwood of Caesalpinia sappan L., could exhibit antioxidant, anti-inflammatory and anti-apoptotic activities. Therefore, we assumed that SA has a potential use for preventing against MIRI. The present study aimed to investigate the effect of SA treatment on MIRI and its mechanism. Cardiomyocytes (H9c2 cells) were treated with SA for 1 h, followed by 6 h of hypoxia/3 h of reoxygenation. Cell viability assay was detected by CCK-8 assay. Apoptosis was measured by flow cytometry and Hoechst staining. Mitochondrial permeability transition pore (mPTP) opening and mitochondrial transmembrane potential (ΔΨm) were measured by spectrophotometry and JC-1 staining. The changes of mitochondrial apoptosis-related proteins and PI3K-Akt-Gsk-3β signaling pathway were evaluated by Western blotting. The results showed that SA pretreatment enhanced the cell viability and decreased the activity of myocardial enzyme in a dose-dependent manner. Moreover, SA pretreatment significantly inhibited apoptosis, blocked mPTP opening, suppressed the release of ΔΨm, prevented the cytochrome c releasing from mitochondria into cytoplasm, and repressed the cleavage of caspase-9 and caspase-3. Furthermore, SA pretreatment increased the phosphorylation levels of Akt and Gsk-3β but not of Stat-3. Meanwhile, the protective effect of SA was abrogated by PI3K inhibitor (LY294002). In conclusion, our results demonstrate that SA could prevent hypoxia/reoxygenation-induced cardiomyocytes injury through inhibition of mitochondrial apoptosis and activation of PI3K-Akt-Gsk-3β pathway. Thus, SA may have a potential use for the prevention of MIRI.
© 2020 The Author(s).
Apoptosis; Mitochondrial apoptosis pathway; Myocardial ischemia reperfusion injury; PI3K-Akt-Gsk-3β pathway; Sappanone A
Sappanone A alleviates hypoxia/reoxygenation-induced cardiomyocytes injury through inhibition of mitochondrial apoptosis and activation of PI3K-Akt-Gsk-3β pathway.
Shi X1, Tao G1, Ji L1, Tian G1.
2020 Feb 28
Oxidative stress is a major contributor to the onset and development of myocardial ischemia reperfusion injury (MIRI). Sappanone A (SA), a homoisoflavanone extracted from the heartwood of Caesalpinia sappan L., has been demonstrated to possess powerful antioxidant activity. Therefore, this study aimed to determine the protective effect of SA on MIRI and investigate its underlying mechanism.
The rat hearts were isolated and underwent 30-min ischemia, followed by 120-min reperfusion to establish the MIRI model, using the Langendorff method. SA was administrated intraperitoneally into rats 1 h prior to heart isolation. The myocardial infarct size and apoptosis were measured by TTC and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Myocardial enzyme activity, MDA content and the activities of SOD and GSH-Px were detected by colorimetric spectrophotometric method. Reactive oxygen species (ROS) level was detected by DCFH-DA probe. The change in Keap1/Nrf2 signaling pathway was evaluated by Western blotting.
SA reduced myocardial infarct size and the release of CK-MB and LDH in a dose-dependent manner. Moreover, SA improved the recovery of cardiac function, inhibited MIRI-induced apoptosis, repressed the production of ROS and MDA, and enhanced the activities of SOD and GSH-Px. Mechanistically, SA downregulated Keap1, induced Nrf2 nuclear accumulation, and enhanced Nrf2 transcriptional activity, subsequently resulting in an increase in the expression of the Nrf2 target genes heme oxygenase-1 and NAD(P)H quinone dehydrogenase 1. Moreover, SA enhanced the phosphorylation of Nfr2, but the enhancement in Nfr2 phosphorylation was abrogated by PKC or PI3K inhibitor.
Collectively, it was demonstrated that SA prevents MIRI via coordinating the cellular antioxidant defenses and maintaining the redox balance, by modulation of Nrf2 via the PKC or PI3K pathway. Therefore, SA was a potential therapeutic drug for treating MIRI.
© 2020 Shi et al.
Nrf2; Sappanone A; apoptosis; myocardial ischemia reperfusion injury; oxidative stress
Sappanone A Protects Against Myocardial Ischemia Reperfusion Injury by Modulation of Nrf2.
Shi X1, Tao G1, Ji L1, Tian G1.
2020 Jan 8
We aimed to explore the effect of Sappanone A on neurologic damage induced by hypoxia.
PC-12 cells were pre-treated with Sappanone A and were simulated by hypoxia. miRNA transfection was performed to overexpress or suppress the expression of miR-15a in PC-12 cells. Cell viability, apoptosis, migration, and expression levels of miR-15a were tested to evaluate the in vitro impact of Sappanone A on hypoxia-injured PC-12 cells.
Hypoxia exposure induced a significant damage in PC-12 cells, as evidenced by the repressed cell growth, the induced apoptosis and the impaired migrating capacity. Sappanone A pretreatment protected PC-12 cells against hypoxia-mediated cell damage. More interestingly, Sappanone A treatment down-regulated miR-15a, and the neuroprotective effects of Sappanone A were attenuated by miR-15a overexpression while were accelerated by miR-15a suppression. Finally, Sappanone A significantly activated Wnt/β-catenin and PI3K/AKT signaling pathways. And the activation of these two signaling induced by Sappanone A were repressed by miR-15a overexpression and were enhanced by miR-15a suppression.
Sappanone A exerted protective activity in PC-12 cells which were stimulated by hypoxia. One of the possible mechanisms of the neuroprotective effect is that: Sappanone A down-regulated the expression of miR-15a, and thus activated Wnt/β-catenin and PI3K/AKT signaling pathways.
Copyright © 2018. Published by Elsevier B.V.
Cerebral ischemia; Hypoxia; Sappanone A
Sappanone A prevents hypoxia-induced injury in PC-12 cells by down-regulation of miR-15a.
Kang C1, Gao J2, Kang M3, Liu X1, Fu Y2, Wang L4.
2019 Feb 15