Sonodynamic Therapy Inhibits Fibrogenesis in Rat Cardiac Fibroblasts Induced by TGF-β1

• Main Authors: Yuanyuan Guo, Zengxiang Dong, Yuanqi Shi, Wei Wang, Lu Wang, Jing Sun, Xin Sun, Zhen Tian, Jianting Yao, Zhitao Li, Jiali Cheng, Ye Tian
• Format: Article
• Language: English
• Published: Cell Physiol Biochem Press GmbH & Co KG 2016-11-01
• Series: Cellular Physiology and Biochemistry
• Subjects: SDT; Cardiac fibroblast; TGF-β1; GSK3β; AKT
• Online Access: http://www.karger.com/Article/FullText/452571

Background/Aims: Sonodynamic therapy (SDT) is a localized ultrasound-activated therapy for atherosclerosis when combined with a sonosensitizer, 5-aminolevulinic acid (ALA), but whether it can prevent cardiac fibrosis has not been studied. In the present study, we evaluated the effects SDT on fibrogenesis in rat cardiac fibroblasts. Methods: The primary cardiac fibroblasts were isolated from rats, and induced to fibrogenesis with TGF-β1. With this in vitro model, we tested the preventive effects of SDT on fibrogenesis and further the underlying mechanism. Results: TGF-β1 stimulation up-regulated α-SMA and COLI/III protein levels in cardiac fibroblasts, and enhanced the progression of cells from the G0/G1 phase to the S phase. SDT inhibited the TGF-β1 mediated cell proliferation and decreased the levels of α-SMA and COLI/III by activating AKT/GSK3β pathway and blocking TGF-β1/SMAD3 signaling. Conclusion: Our studies demonstrate an antifibrotic effect of SDT in rat cardiac fibroblasts, suggesting that SDT may intervene cardiac fibrogenesis by regulating myocardial fibrotic remodeling.