通讯作者: 陈徐波, 18867922539@163.com

DOI：10.12201/bmr.202506.00013

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

• 摘要：目的：基于音猬因子（Sonic hedgehog，Shh）/神经胶质瘤相关致癌基因同系物1（Glioma-Associated Oncogene 1，Gli1）信号通路探讨虎杖苷（Polydatin，PD）对阿霉素诱导扩张型心肌病（Dilated cardiomyopathy，DCM）大鼠心肌损伤的影响。方法：将SD大鼠随机分为Con组、DCM组、PD低剂量组、PD中剂量组、PD高剂量组、Cyclopamine组，每组10只。除Con组外，其余组均通过阿霉素诱导构建DCM大鼠模型。检测各组大鼠心功能指标；观察大鼠心肌组织病理、纤维化改变及心肌细胞凋亡；检测大鼠血清炎性相关因子水平；检测心肌组织Ⅰ型胶原和Ⅲ型胶原表达；检测各组大鼠心肌组织Shh/Gli1信号通路蛋白表达。结果：DCM组与Con组比较，大鼠心肌组织病理损伤和纤维化严重，心脏左室收缩末期内径（Left Ventricular End-Systolic Diameter，LVESD）、左室舒张末期内径（Left ventricular end diastolic dimension，LVEDD）、心肌细胞凋亡率、白细胞介素1β（Interleukin-1β，IL-1β）、白细胞介素18（Interleukin-18，IL-18）、Ⅰ型胶原、Ⅲ型胶原平均光密度值增加（P＜0.05），左室射血分数（Left Ventricular Ejection Fraction，LVEF）、左室短轴缩短率（Left Ventricular Fractional Shortening，FS）、Shh、Gli1表达降低（P＜0.05）；PD低剂量组、PD中剂量组、PD高剂量组与DCM组比较，大鼠心肌组织病理损伤和纤维化减轻，LVESD、LVEDD、心肌细胞凋亡率、IL-1β、IL-18、Ⅰ型胶原、Ⅲ型胶原平均光密度值减少（P＜0.05），LVEF、FS、Shh、Gli1表达增加（P＜0.05）；Cyclopamine组与PD高剂量组比较，大鼠心肌组织病理损伤和纤维化加重，LVESD、LVEDD、心肌细胞凋亡率、IL-1β、IL-18、Ⅰ型胶原、Ⅲ型胶原平均光密度值显著增加（P＜0.05），LVEF、FS、Shh、Gli1表达显著减少（P＜0.05）。结论：PD可能通过激活Shh/Gli1信号通路能够改善阿霉素诱导DCM大鼠心肌损伤。

  关键词： 虎杖苷；音猬因子/神经胶质瘤相关致癌基因同系物1；扩张型心肌病；心肌损伤; ; ; 

   

  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

  提交时间：2025-06-05

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• 序号	提交日期	编号	操作
  1	2025-04-25	bmr.202506.00013V1	下载

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