Planta Med 2019; 85(05): 360-369
DOI: 10.1055/a-0791-1049
Biological and Pharmacological Activity
Original Papers
Georg Thieme Verlag KG Stuttgart · New York

Baicalin Induces Apoptotic Death of Human Chondrosarcoma Cells through Mitochondrial Dysfunction and Downregulation of the PI3K/Akt/mTOR Pathway

Minyu Zhu
Department of Spine Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China
,
Jinwei Ying
Department of Spine Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China
,
Chaowei Lin
Department of Spine Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China
,
Yu Wang
Department of Spine Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China
,
Kelun Huang
Department of Spine Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China
,
Yang Zhou
Department of Spine Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China
,
Honglin Teng
Department of Spine Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China
› Author Affiliations
Further Information

Publication History

received 29 June 2018
revised 25 October 2018

accepted 05 November 2018

Publication Date:
23 November 2018 (online)

Abstract

The aim of the present study was to investigate the cytotoxic and antitumour effects of baicalin in human chondrosarcoma both in vivo and in vitro. We examined the effects of baicalin on the growth and apoptosis of human chondrosarcoma cells. Baicalin inhibited the growth of SW1353 and CH2879 cells in a dose- and time-dependent manner, but did not inhibit the growth of normal chondrocytes. Baicalin reduced tumour growth and induced apoptotic death in SW1353-transplanted nude mice without reducing their body weight. Further studies showed that baicalin reduced the mitochondrial membrane potential, upregulated the expression of Bax and cytoplasmic cytochrome c, downregulated the expression of Bcl-2 and mitochondrial cytochromes, and activated caspase-3 and caspase-9. Baicalin inhibited the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathway by decreasing the expression of phosphorylated phosphoinositide 3-kinase, phosphorylated protein kinase B, and phosphorylated mammalian target of rapamycin both in vivo and in vitro. Moreover, the mice that received SC79 and baicalin exhibited a greater tumour size compared with the mice that received baicalin. The mice that received LY294002 and baicalin showed a smaller tumour size compared with the mice that received baicalin. In the in vitro study, SC79 and LY294002 affected the baicalin-induced cytotoxic effects on chondrosarcoma cells in the same manner. Our data suggest baicalin has therapeutic efficacy in human chondrosarcoma through the induction of apoptosis and inhibition of the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathway. Baicalin can be considered a potential therapeutic agent for treating chondrosarcomas.

Supporting Information

 
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