Baicalin administration attenuates hyperglycemia-induced malformation of cardiovascular system

Guang Wang, Jianxin Liang, Lin-Rui Gao, Zhen-Peng Si, Xiao-Tan Zhang, Guo Liang, Yu Yan, Ke Li, Xin Cheng, Yongping Bao, Manli Chuai, Li-Guo Chen, Da-Xiang Lu, Xuesong Yang

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In this study, the effects of Baicalin on the hyperglycemia-induced cardiovascular malformation during embryo development were investigated. Using early chick embryos, an optimal concentration of Baicalin (6 μM), was identified which could prevent hyperglycemia-induced cardiovascular malformation of embryos. Hyperglycemia-enhanced cell apoptosis was reduced in embryos and HUVECs in the presence of Baicalin. Hyperglycemia-induced excessive ROS production was inhibited when Baicalin was administered. Analyses of SOD, GSH-Px, MAQE and GABAA suggested Baicalin plays an antioxidant role in chick embryos possibly through suppression of outwardly rectifying Cl(-) in the high-glucose microenvironment. In addition, hyperglycemia-enhanced autophagy fell in the presence of Baicalin, through affecting the ubiquitin of p62 and accelerating autophagy flux. Both Baicalin and Vitamin C could decrease apoptosis, but CQ did not, suggesting autophagy to be a protective function on the cell survival. In mice, Baicalin reduced the elevated blood glucose level caused by streptozotocin (STZ). Taken together, these data suggest that hyperglycemia-induced embryonic cardiovascular malformation can be attenuated by Baicalin administration through suppressing the excessive production of ROS and autophagy. Baicalin could be a potential candidate drug for women suffering from gestational diabetes mellitus.
Original languageEnglish
Article number234
JournalCell Death & Disease
Publication statusPublished - 14 Feb 2018


  • Baicalin
  • angiogenesis
  • heart tube formation
  • apoptosis
  • ROS

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