Icariin ameliorates heart failure by attenuating ferroptosis through the upregu-lation of the SLC7A11/GPX4 axis
Objective To study the mechanism of Icariin anti-isoproterenol induced heart failure in mice based on lipid peroxidation inhibition.Methods C57BL/6 mices were randomly divided into a control group,an iso-proterenol model group(ISO,15 mg/kg),a losartan positive drug group(Los,9 mg/kg),a low-dose Icariin group(ICA-L group,15 mg/kg),and a high-dose Icariin group(ICA-H group,60 mg/kg).Small animal ul-trasound detector was used to detect changes in mouse heart function;the mouse heart index was calculated;HE staining was used to observe the pathological changes in the left ventricular tissue of mice;Bruce blue was used to stain the accumulation of iron ions in the left ventricular tissue of mice;Western blot was used to detect the expression of iron death related proteins(SLC7A11,GPX4,4-HNE,ACSL4,LPCAT3,TFR1,DMT1)in mouse left ventricular tissue.Results ICA and Los improved the ISO-decreased left ventricular ejection fraction(EF％)and left ventricular fractional shortening(FS％),alleviated the pathological damage and excessive ac-cumulation of iron ions in the left ventricular tissue caused by ISO,inhibited the downregulation of SLC7A11 and GPX4 proteins in the left ventricular tissue caused by ISO,and upregulated 4-HNE,ACSL4,LPCAT3,TFR1 and DMT1 proteins(P＜0.05).Conclusion ICA upregulates the SLC7A11/GPX4 axis against lipid peroxida-tion,attenuating ferroptosis improves heart failure in mice.
icariinheart failureferroptosissolute carrier family 7 member 11glutathione peroxidase 4
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维普
