Evidence map›Paper›PMID 29445081›Full record

ArticleCell death & disease2018

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 and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 2 countries.

Guang WangDivision of Histology & Embryology, Joint Laboratory for Embryonic Development & Prenatal Medicine, Medical College, Jinan University, Guangzhou, 510632, China.
Jianxin LiangDivision of Histology & Embryology, Joint Laboratory for Embryonic Development & Prenatal Medicine, Medical College, Jinan University, Guangzhou, 510632, China.
Lin-Rui GaoDivision of Histology & Embryology, Joint Laboratory for Embryonic Development & Prenatal Medicine, Medical College, Jinan University, Guangzhou, 510632, China.
Zhen-Peng SiDepartment of Pediatrics and Neonatology, Institute of Fetal-Preterm Labor Medicine; The First Affiliated Hospital, Jinan University, Guangzhou, 510630, China.
Xiao-Tan ZhangDivision of Histology & Embryology, Joint Laboratory for Embryonic Development & Prenatal Medicine, Medical College, Jinan University, Guangzhou, 510632, China.
Guo LiangDivision of Histology & Embryology, Joint Laboratory for Embryonic Development & Prenatal Medicine, Medical College, Jinan University, Guangzhou, 510632, China.
Yu YanDivision of Histology & Embryology, Joint Laboratory for Embryonic Development & Prenatal Medicine, Medical College, Jinan University, Guangzhou, 510632, China.
Ke LiDivision of Histology & Embryology, Joint Laboratory for Embryonic Development & Prenatal Medicine, Medical College, Jinan University, Guangzhou, 510632, China.
Xin ChengDivision of Histology & Embryology, Joint Laboratory for Embryonic Development & Prenatal Medicine, Medical College, Jinan University, Guangzhou, 510632, China.
Yongping BaoNorwich Medical School, University of East Anglia, Norwich, Norfolk, UK.
Manli ChuaiDivision of Cell and Developmental Biology, University of Dundee, Dundee, DD1 5EH, UK.
Li-Guo ChenChinese Medicine College, Jinan University, Guangzhou, 510632, China.
Da-Xiang LuDepartment of Pathophysiology, Institute of Brain Research, Medical College, Jinan University, Guangzhou, 510632, China.
Xuesong YangDivision of Histology & Embryology, Joint Laboratory for Embryonic Development & Prenatal Medicine, Medical College, Jinan University, Guangzhou, 510632, China. yang_xuesong@126.com.
Jinan University · CNFirst Affiliated Hospital of Jinan University · CNUniversity of Dundee · GBUniversity of East Anglia · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AnimalsAntioxidantsAscorbic AcidAutophagyBlood GlucoseCardiovascular SystemChick EmbryoChloride ChannelsDiabetes Mellitus, ExperimentalEmbryo, NonmammalianFemaleFlavonoidsGene Expression RegulationGlutathione PeroxidaseHumansHuman Umbilical Vein Endothelial CellsAntioxidantsAscorbic AcidbaicalinBlood GlucoseChloride ChannelsFlavonoidsGlutathione PeroxidaseHypoglycemic AgentsSequestosome-1 ProteinSqstm1 protein, mouseStreptozocinSuperoxide Dismutase

Identifiers

PMID29445081
PMCPMC5833405
OpenAlexW2790255831

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.