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

doi:10.1038/s41419-018-0318-2

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 (Lead / Corresponding author)

Research output: Contribution to journal › Article › peer-review

66 Citations (Scopus)

327 Downloads (Pure)

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.

Original language	English
Article number	234
Pages (from-to)	1-17
Number of pages	17
Journal	Cell Death and Disease
Volume	9
Issue number	2
DOIs	https://doi.org/10.1038/s41419-018-0318-2
Publication status	Published - 14 Feb 2018

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

ASJC Scopus subject areas

Immunology
Cellular and Molecular Neuroscience
Cell Biology
Cancer Research

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Cite this

@article{08d4d13a9c444f7080974a8a7134669f,

title = "Baicalin administration attenuates hyperglycemia-induced malformation of cardiovascular system",

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.",

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

note = "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).",

year = "2018",

month = feb,

day = "14",

doi = "10.1038/s41419-018-0318-2",

language = "English",

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journal = "Cell Death and Disease",

issn = "2041-4889",

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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 -

Baicalin administration attenuates hyperglycemia-induced malformation of cardiovascular system

Abstract

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