Evidence map›Paper›PMID 33421306›Full record

ArticlePharmacology research & perspectives2021

Protective effect of baicalin against pulmonary arterial hypertension vascular remodeling through regulation of TNF-α signaling pathway.

Xia Xue, Shanshan Zhang, Wen Jiang, Jue Wang, Qian Xin, Chao Sun, Kailin Li, Tonggang Qi, Yun Luan

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pharmacology research & perspectives, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 29 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

9 authors at 1 institution in 1 country.

Xia XueDepartment of Pharmacy, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Shanshan ZhangDepartment of Emergency, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Wen JiangCentral Research Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Jue WangCentral Research Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Qian XinCentral Research Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Chao SunCentral Research Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Kailin LiCentral Research Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Tonggang QiCentral Research Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Yun LuanCentral Research Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.ORCID 0000-0001-6149-8226
Second Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a progressive cardiovascular disease with high mortality. However, there were no efficient medical drugs for PAH to enormously improve the survival and quality of life measures. The present study aimed to explore the protective effect of baicalin against experimental PAH in vivo and vitro. All the experimental rats received intraperitoneal injection of monocrotaline (MCT) to induce PAH model. Baicalin was given by intragastric administration from 2 days after MCT injection. Forty animals were randomly divided into four groups: Control, MCT, saline-, and baicalin-treated groups (n = 10 in each). Post-operation, hemodynamic data, and index of right ventricular hypertrophy (RVHI) were recorded to evaluate the inhibition of baicalin on MCT-induced PAH. Furthermore, pulmonary artery smooth muscle cells (PASMCs) model induced by tumor necrosis factor-α (TNF-α) was used to observe the inhibition of vascular cells proliferation in vitro. The results demonstrated that baicalin significantly attenuated MCT-induced right ventricular systolic pressure (RVSP), the index of right ventricular hypertrophy, and vessel wall thickness; inhibit inflammatory and cell proliferation induced by MCT or TNF-α, respectively. In addition, we found that baicalin might protect against experimental PAH via regulating the TNF-α/BMPR2 signaling pathway.

Indexed as

ActinsAnimalsAntihypertensive AgentsBone Morphogenetic Protein Receptors, Type IICell MovementCell ProliferationCells, CulturedFlavonoidsInterleukin-1betaInterleukin-6LungMaleMyocytes, Smooth MusclePulmonary Arterial HypertensionRatsRats, WistarActa2 protein, ratActinsAntihypertensive AgentsbaicalinBmpr2 protein, ratBone Morphogenetic Protein Receptors, Type IIFlavonoidsIL1B protein, ratIl6 protein, ratInterleukin-1betaInterleukin-6Smad ProteinsTumor Necrosis Factor-alphaBaicalinBMPR2PAHTNF-αVascular remodeling

Identifiers

PMID33421306
PMCPMC7796790
OpenAlexW3120716302

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.