TY - JOUR
T1 - Baicalin administration attenuates hyperglycemia-induced malformation of cardiovascular system
AU - Wang, Guang
AU - Liang, Jianxin
AU - Gao, Lin-Rui
AU - Si, Zhen-Peng
AU - Zhang, Xiao-Tan
AU - Liang, Guo
AU - Yan, Yu
AU - Li, Ke
AU - Cheng, Xin
AU - Bao, Yongping
AU - Chuai, Manli
AU - Chen, Li-Guo
AU - Lu, Da-Xiang
AU - Yang, Xuesong
N1 - This study was supported by the NSFC grant (81741016, 31771331), Science and Technology Planning Project of Guangdong Province (2014A020221091, 2017A020214015, 2017A050506029, 2016B030229002, 2014A020213008), Science and Technology Program of Guangzhou (201710010054), China Postdoctoral Science Foundation (2015T80940), Guangdong Natural Science Foundation (2016A030311044), The Fundamental Research Funds for the Central Universities (21617466), The Funds for Young Creative Talents of Higher Education in Guangdong Province (2014KQNCX026) and Research Grant of Key Laboratory of Regenerative Medicine, Ministry of Education, Jinan University (No. ZSYX-M-00001 and ZSYX-T-00001).
PY - 2018/2/14
Y1 - 2018/2/14
N2 - 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, MQAE 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.
AB - 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, MQAE 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.
U2 - 10.1038/s41419-018-0318-2
DO - 10.1038/s41419-018-0318-2
M3 - Article
C2 - 29445081
SN - 2041-4889
VL - 9
SP - 1
EP - 17
JO - Cell Death and Disease
JF - Cell Death and Disease
IS - 2
M1 - 234
ER -