Evidence map›Paper›PMID 31723406›Full record

ArticlePulmonary circulation

Baicalin prevents pulmonary arterial remodeling in vivo via the AKT/ERK/NF-κB signaling pathways.

Guosen Yan, Jinxia Wang, Tao Yi, Junfen Cheng, Haixu Guo, Yuan He, Xiaorong Shui, Zeyong Wu, Shian Huang, Wei Lei

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Pulmonary circulation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 22 citations in OpenAlex.

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  11. Baicalin and lung diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Guosen YanLaboratory of Cardiovascular Diseases, Guangdong Medical University, Zhanjiang, China.
Jinxia WangLaboratory of Cardiovascular Diseases, Guangdong Medical University, Zhanjiang, China.
Tao YiLaboratory of Cardiovascular Diseases, Guangdong Medical University, Zhanjiang, China.
Junfen ChengDepartment of Respiration, the Second Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Haixu GuoLaboratory of Cardiovascular Diseases, Guangdong Medical University, Zhanjiang, China.
Yuan HeLaboratory of Cardiovascular Diseases, Guangdong Medical University, Zhanjiang, China.
Xiaorong ShuiLaboratory of Vascular Surgery, Guangdong Medical University, Zhanjiang, China.
Zeyong WuDepartment of Plastic Surgery, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Shian HuangCardiovascular Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Wei LeiLaboratory of Cardiovascular Diseases, Guangdong Medical University, Zhanjiang, China.
Guangdong Medical College · CNAffiliated Hospital of Guangdong Medical College Hospital · CNSecond Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension is a rapidly progressive and often fatal disease. As the pathogenesis of pulmonary arterial hypertension remains unclear, there is currently no good drug for pulmonary arterial hypertension and new therapy is desperately needed. This study investigated the effects and mechanism of baicalin on vascular remodeling in rats with pulmonary arterial hypertension. A rat pulmonary arterial hypertension model was constructed using intraperitoneal injection of monocrotaline, and different doses of baicalin were used to treat these rats. The mean pulmonary arterial pressure (mPAP) and right ventricular systolic pressure (RVSP) were measured with a right heart catheter. Moreover, the hearts were dissected to determine the right ventricular hypertrophy index (RVHI). The lung tissues were stained with H&E and Masson's staining to estimate the pulmonary vascular remodeling and collagen fibrosis, and the expression of proteins in the AKT, ERK, and NF-κB p65 phosphorylation (p-AKT, p-ERK, p-p65) was examined by Western blot analysis. We found that compared with untreated pulmonary arterial hypertension rats, baicalin ameliorated pulmonary vascular remodeling and cardiorespiratory injury, inhibited p-p65 and p-ERK expression, and promoted p-AKT and p-eNOS expression. In conclusion, baicalin interfered with pulmonary vascular remodeling and pulmonary arterial hypertension development in rats through the AKT/eNOS, ERK and NF-κB signaling pathways.

Indexed as

baicalininflammationproliferationpulmonary arterial hypertensionvascular remodeling

Identifiers

PMID31723406
PMCPMC6831981
OpenAlexW2972646943

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.