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Cell Death Dis. 2018 Feb 14;9(2):234. doi: 10.1038/s41419-018-0318-2.

Baicalin administration attenuates hyperglycemia-induced malformation of cardiovascular system.

Author information

1
Division of Histology & Embryology, Joint Laboratory for Embryonic Development & Prenatal Medicine, Medical College, Jinan University, Guangzhou, 510632, China.
2
Chinese Medicine College, Jinan University, Guangzhou, 510632, China.
3
Key Laboratory for Regenerative Medicine of the Ministry of Education, Jinan University, Guangzhou, 510632, China.
4
Department of Pediatrics and Neonatology, Institute of Fetal-Preterm Labor Medicine; The First Affiliated Hospital, Jinan University, Guangzhou, 510630, China.
5
Norwich Medical School, University of East Anglia, Norwich, Norfolk, UK.
6
Division of Cell and Developmental Biology, University of Dundee, Dundee, DD1 5EH, UK.
7
Department of Pathophysiology, Institute of Brain Research, Medical College, Jinan University, Guangzhou, 510632, China.
8
Division of Histology & Embryology, Joint Laboratory for Embryonic Development & Prenatal Medicine, Medical College, Jinan University, Guangzhou, 510632, China. yang_xuesong@126.com.
9
Key Laboratory for Regenerative Medicine of the Ministry of Education, Jinan University, Guangzhou, 510632, China. yang_xuesong@126.com.

Abstract

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.

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