Maltol mitigates cisplatin‐evoked cardiotoxicity via inhibiting the PI3K/Akt signaling pathway in rodents in vivo and in vitro

Our current research aims to evaluate the efficiency of a flavor enhancer, maltol (produced by heating ginseng) against cisplatin‐evoked cardiotoxicity by establishing cisplatin‐induced heart injury in vivo and H9C2 rat cardiomyocyte model. The cisplatin‐treated mice at 3 mg/kg for four times on the...

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Veröffentlicht in:Phytotherapy research 2022-04, Vol.36 (4), p.1724-1735
Hauptverfasser: Xing, Jing‐Jing, Mi, Xiao‐Jie, Hou, Jin‐Gang, Cai, En‐Bo, Zheng, Si‐Wen, Wang, Shi‐Han, Wang, Zi, Chen, Chen, Li, Wei
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Sprache:eng
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Zusammenfassung:Our current research aims to evaluate the efficiency of a flavor enhancer, maltol (produced by heating ginseng) against cisplatin‐evoked cardiotoxicity by establishing cisplatin‐induced heart injury in vivo and H9C2 rat cardiomyocyte model. The cisplatin‐treated mice at 3 mg/kg for four times on the 7th, 9th, 11th and 13th day, and in them appeared a serious cardiac damage accompanied with the increase in indicators of heart damage. Multiple exposure of 3 mg/kg for four times of cisplatin increased cardiac cells apoptosis with increased expression of Bax and cleaved‐caspase 3, and decreased expression of Bcl‐2. Interestingly, supplement of maltol at doses of 50 and 100 mg/kg for 15 days significantly suppressed the cardiac disturbance. In cultured H9C2 cells, maltol enhanced PI3K/Akt expression level during cisplatin treatment, and reduced cisplatin‐induced apoptosis. Notably, inhibition of PI3K/Akt by LY294002 and HY‐10249A lessened the efficacy of maltol. In mice, maltol apparently induced PI3K/Akt in heart tissues and protected against cisplatin‐induced cardiotoxicity. In conclusion, maltol exerted the protective effects against cisplatin‐induced cardiotoxicity, at least partially by inhibiting the activation of PI3K/Akt signaling pathways in cardiomyocytes, to ease oxidative stress, and alleviate reactive oxygen species‐mediated apoptosis.
ISSN:0951-418X
1099-1573
DOI:10.1002/ptr.7405