Evidence map›Paper›PMID 31273392›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2019

Baicalin ameliorates lipopolysaccharide-induced acute lung injury in mice by suppressing oxidative stress and inflammation via the activation of the Nrf2-mediated HO-1 signaling pathway.

Xiangli Meng, Lin Hu, Wenqiang Li

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 84 citations in OpenAlex.

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  18. Baicalin and lung diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2024
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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

3 authors at 2 institutions in 1 country.

Xiangli MengIntensive Care Unit (ICU), Affiliated Hospital of Jining Medical University, Shandong Province, Zoucheng District, Jining, 273500, Shandong, People's Republic of China.
Lin HuIntensive Care Unit (ICU), Affiliated Hospital of Jining Medical University, Shandong Province, Zoucheng District, Jining, 273500, Shandong, People's Republic of China.
Wenqiang LiIntensive Care Unit (ICU), Jining No.1 People's Hospital, No.6, Health Road, Jining City, 272011, Shandong Province, People's Republic of China. Liwengqiang70@outlook.com.
Affiliated Hospital of Jining Medical University · CNJining First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This research aims to investigate the ameliorative potential of baicalin on lipopolysaccharide-induced acute lung injury by the suppression of oxidative stress and inflammation via the activation of the nuclear erythroid factor 2 (Nrf2)-mediated heme oxygenase-1 (HO-1) signaling pathway. Specific pathogen-free male mice, weighing between 25 and 30 g, were divided into the following four groups of 10 mice each: the control group, LPS group, LPS + baicalin group, and baicalin group. Bronchoalveolar lavage fluid (BALF), blood, and tissue were collected on the 16th day and used for hematological (total leukocyte, macrophage, neutrophil, and lymphocyte counts in both blood and BALF, biochemical (antioxidant enzymes, MDA, Nrf2, and HO-1), and histological analyses. The protective effect of baicalin on lipopolysaccharide-induced acute lung injury is based on its antioxidative stress capabilities that are mediated partly by the Nrf2/HO-1 signaling pathway. Baicalin pretreatment significantly decreased the rise in the lung injury score; total leukocyte, neutrophil, lymphocyte, and macrophage counts; pro-inflammatory mediators, tumor necrosis factor (TNF-α), interleukins (IL-6 and IL-1β); biosynthesis of oxidative products, e.g., malondialdehyde (MDA); and restoration of antioxidative enzyme (superoxide dismutase and catalase) activities by improving the expression of nuclear Nrf2 and cytosolic HO-1 in lipopolysaccharide-induced acute lung injury. The protective effects of baicalin are partly due to its antioxidant and anti-inflammatory effects. Our findings indicate that baicalin protects against lipopolysaccharide-induced severe lung injury by enhancing antioxidant systems and significantly reducing both inflammatory cells and mediators via the Nrf2-mediated HO-1 signaling pathway.

Indexed as

Acute Lung InjuryAnimalsAntioxidantsBronchoalveolar Lavage FluidCytokinesFlavonoidsHeme Oxygenase-1InflammationLeukocyte CountLipopolysaccharidesMaleMembrane ProteinsMiceNF-E2-Related Factor 2Oxidative StressSignal TransductionAntioxidantsbaicalinCytokinesFlavonoidsHeme Oxygenase-1Hmox1 protein, mouseLipopolysaccharidesMembrane ProteinsNfe2l2 protein, mouseNF-E2-Related Factor 2BaicalinHO-1InflammationLung injuryNrf2Oxidative stress

Identifiers

PMID31273392
OpenAlexW2955666073

What Socratic holds

Textmetadata
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.