Fig. 7: Dihydroartemisinin (DHA) competitively antagonized NPM3-induced H3K18la and H3K27la to inhibit FASN transcription and necroptosis in diabetic cardiomyopathy (DCM) model mice. | Nature Communications

Fig. 7: Dihydroartemisinin (DHA) competitively antagonized NPM3-induced H3K18la and H3K27la to inhibit FASN transcription and necroptosis in diabetic cardiomyopathy (DCM) model mice.

From: NPM3 functions as a lactyltransferase to promote necroptosis in male diabetic cardiomyopathy mice models via FASN transcription modulation

Fig. 7: Dihydroartemisinin (DHA) competitively antagonized NPM3-induced H3K18la and H3K27la to inhibit FASN transcription and necroptosis in diabetic cardiomyopathy (DCM) model mice.The alternative text for this image may have been generated using AI.

a Mice that were administered 20 mg/kg DHA by gavage once a day after the injection of citrate buffer or STZ were designated the DHA group or the DCM + DHA group. Representative images of HE staining, Masson’s trichrome staining and IHC staining for NPM3, H3K18la, H3K27la, FASN, RIPK1, p-RIPK1, MLKL and p-MLKL in cardiac biopsy samples from control (Con), DHA, DCM and DCM + DHA model mice (scale bar: 50 μm). Compared with DCM model mice, DCM + DHA model mice presented lower levels of NPM3, H3K18la, H3K27la and FASN; less necroptosis; and less heart injury and interstitial fibrosis (n = 8). b Western blotting revealed that DHA treatment decreased the levels of NPM3, H3K18la, H3K27la and FASN and attenuated necroptosis in the hearts of DCM model mice. c qPCR assays indicated that DHA treatment decreased the NPM3 mRNA level in the hearts of DCM model mice (n = 8). d qPCR assays indicated that DHA treatment decreased FASN mRNA levels in the hearts of DCM model mice (n = 8). e Representative micrographs of PW Doppler echocardiography. f Representative micrographs of M-Mode echocardiography data. g Left ventricular (LV) mass was evaluated. Compared with DCM model mice, DCM + DHA model mice presented a reduced LV mass (n = 8). h The MV E/A ratio was evaluated. Compared with DCM model mice, DCM + DHA model mice presented less diastolic dysfunction (n = 8). i The MV E/E’ ratio was evaluated. Compared with DCM model mice, DCM + DHA model mice presented less diastolic dysfunction (n = 8). j Evaluation of systolic function by left ventricular ejection function (LVEF). No significant changes in LVEF were detected between DCM model mice and DCM + DHA model mice (n = 8). Data are presented as mean values ± SD. Two-sided unpaired t-test was performed in (a, c, d, g–j) and presented as *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Source data, including exact P values are provided as a Source Data file.

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