The effect of polydatin on myocardial injury in rats with doxorubicin induced dilated cardiomyopathy by regulating the Shh/Gli1 signaling pathway

DOI: 10.12201/bmr.202506.00013

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  Abstract: To discuss the effect of polydatin (PD) on myocardial injury in rats with doxorubicin induced dilated cardiomyopathy (DCM) based on the sonic hedgehog (Sonic hedgehog, Shh)/glioma-associated oncogene homolog 1 (Gli1) signaling pathway. Methods: SD rats were assigned into Con group, DCM group, low-dose PD group, medium-dose PD group, high-dose PD group, and Cyclopamine group randomly, each with 10 rats. Except for the Con group, all other groups were induced to construct DCM rat models using doxorubicin. The cardiac function indicators of rats in each group were tested. The pathological changes of myocardial tissue, fibrosis and myocardial cell apoptosis were observed. The levels of inflammatory related factors in serum were detected. The expression of type Ⅰ collagen and type Ⅲ collagen in myocardial tissue was detected. The protein expression of Shh/Gli1 signaling pathway in myocardial tissue was detected. Results: Compared with the Con group, the DCM group showed severe pathological damage and fibrosis in rat myocardial tissue, the left ventricular end systolic diameter ( LVESD), left ventricular end diastolic diameter (LVEDD), myocardial cell apoptosis rate, Interleukin-1β(IL-1β), (Interleukin-18, IL-18), and the average optical density values of type I collagen and type III collagen increased (P<0.05), while the left ventricular ejection fraction (LVEF), left ventricular fractional shortening (FS), Shh, and Gli1 decreased (P<0.05). Compared with the DCM group, the low-dose PD group, medium-dose PD group, and high-dose PD group showed reduced pathological damage and fibrosis in rat myocardial tissue, the LVESD, LVEDD, myocardial cell apoptosis rate, IL-1β, IL-18, and the average optical density values of type I collagen and type III collagen decreased (P<0.05), while the LVEF, FS, Shh, and Gli1 increased (P<0.05). Compared with the high-dose PD group, the Cyclopamine group showed aggravated pathological damage and fibrosis in rat myocardial tissue, the LVESD, LVEDD, myocardial cell apoptosis rate, IL-1β, IL-18, and the average optical density values of type I collagen and type III collagen increased (P<0.05), while the LVEF, FS, Shh, and Gli1 decreased (P<0.05). Conclusion: PD may improve doxorubicin induced myocardial injury in DCM rats by activating Shh/Gli1 signaling pathway.

  Key words: Polydatin; Sonic hedgehog/glioma-associated oncogene homolog 1; Dilated cardiomyopathy; Myocardial injury

  Submit time: 5 June 2025

  Copyright: The copyright holder for this preprint is the author/funder, who has granted biomedRxiv a license to display the preprint in perpetuity.
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