Evidence map›Paper›PMID 34250720›Full record

ArticleThe Kaohsiung journal of medical sciences2021

Hypaphorine exerts anti-inflammatory effects in sepsis induced acute lung injury via modulating DUSP1/p38/JNK pathway.

Yu-Hua Ding, Run-Xin Miao, Qiang Zhang

Open access · goldAbstract read
In one paragraph

Article in The Kaohsiung journal of medical sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Phytochemical Profile and Antioxidant Potential ofAntioxidants (Basel, Switzerland) · 2026
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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 1 institution in 1 country.

Yu-Hua DingDepartment of Pharmacy, Zaozhuang Hospital of Traditional Chinese Medicine, Zaozhuang, Shandong, China.
Run-Xin MiaoDepartment of Emergency, Zaozhuang Hospital of Traditional Chinese Medicine, Zaozhuang, Shandong, China.
Qiang ZhangDepartment of Pharmacy, Zaozhuang Hospital of Traditional Chinese Medicine, Zaozhuang, Shandong, China.ORCID https://orcid.org/0000-0002-7248-6244
Zaozhuang Municipal Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is a systemic inflammatory response syndrome attributed to infection, while sepsis-induced acute lung injury (ALI) has high morbidity and mortality. Here, we aimed to explore the specific mechanism of hypaphorine's anti-inflammatory effects in ALI. Lipopolysaccharide (LPS) was adopted to construct ALI model both in vivo and in vitro. BEAS-2B cell viability and apoptosis was testified by the MTT assay and flow cytometry. Reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) were performed to examine the expression of proinflammatory cytokines (IL-1β, IL-6, TNF-α, and IL-18), and Western blot was adopted to examine the expression of the apoptosis-related proteins (Bax, Bcl2, and Caspase3) and the DUSP1/p38/JNK signaling pathway. At the same time, lung injury score, lactate dehydrogenase (LDH) and myeloperoxidase (MPO) activity were monitored. The dry/wet weight method was used to examine lung edema, and the total protein content in BALF was determined to test pulmonary vascular permeability. As the data suggested, hypaphorine inhibited the LPS-mediated apoptosis of alveolar epithelial cells. What is more, hypaphorine attenuated the expression of inflammatory factors (IL-1β, IL-6, TNF-α, and IL-18) and inactivated the p38/JNK signaling pathway through upregulating DUSP1 in a dose-dependent manner. Meanwhile, DUSP1 knockdown weakened the anti-inflammatory effect of hypaphorine on LPS-mediated lung injury. Furthermore, hypaphorine also relieved LPS induced ALI in rats with anti-inflammatory effects. Taken together, hypaphorine prevented LPS-mediated ALI and proinflammatory response via inactivating the p38/JNK signaling pathway by upregulating DUSP1.

Indexed as

Acute Lung InjuryAnimalsAnti-Inflammatory AgentsCell LineDual Specificity Phosphatase 1IndolesMaleMAP Kinase Kinase 4Proto-Oncogene Proteins c-aktRatsRats, Sprague-DawleySepsisAnti-Inflammatory AgentsDual Specificity Phosphatase 1Dusp1 protein, ratIndoleslenticinMAP Kinase Kinase 4Proto-Oncogene Proteins c-aktacute lung injurydual-specific phosphatase 1hypaphorineinflammationsepsis

Identifiers

PMID34250720
PMCPMC11896452
OpenAlexW3179969125

What OpenQuestion 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 OpenQuestion graph.