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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: TFEB-NF-κB inflammatory signaling axis: a novel therapeutic pathway of Dihydrotanshinone I in doxorubicin-induced cardiotoxicity

Fig. 1

DHT improved cardiac function and protected against pathological injury in zebrafish and in mice. a Microscopic examination showed that DHT preserved the heart atrium, and protected against extensive pericardial edema and blood accumulation in tail. By using a high-speed camera, results and analysis showed that DHT increased FS values (b) and blood flow (d). DHT could improve heart rate (c) and survival rate (e). f M-mode echocardiography was assessed to detect cardiac function in each group. g Echocardiography data showed that DHT increased EF% and FS%, and decreased LVEDD and LVESD. h HE staining showed that DHT protected against the structural damage caused by DOX, scale bar = 20 μm. i Quantification of inflammatory cell infiltration (%) showed that DHT decreased the inflammatory cell rate. j Quantification of SOD and MDA levels in plasma. N ≥ 10 per group in zebrafish; N ≥ 5 per group in mice. All data were presented as means ± SD in triplicate. *p < 0.05, **p < 0.01, ***p < 0.001 is significantly different as indicated, for values in the DOX group

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