Evidence map›Paper›PMID 31396818›Full record

ArticleJournal of physiology and biochemistry2019

Baicalin relieves inflammation stimulated by lipopolysaccharide via upregulating TUG1 in liver cells.

Yanqiu Huang, Mengyan Sun, Xuefang Yang, Aiyu Ma, Yujie Ma, Aiying Zhao

RetractedAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Journal of physiology and biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.3field-weighted citation impact, top 9% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Baicalin Attenuates Continuous Activation ofEvidence-based complementary and alternative medicine : eCAM · 2022
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Yanqiu HuangDepartment of Infectious Diseases, Heze Municipal Hospital, No2888 Caozhou Road, Heze, 274000, Shandong, China.
Mengyan SunDepartment of Clinical Laboratory, Heze Municipal Hospital, Heze, 274000, China.
Xuefang YangDepartment of Clinical Laboratory, Heze Municipal Hospital, Heze, 274000, China.
Aiyu MaDepartment of Infectious Diseases, Heze Municipal Hospital, No2888 Caozhou Road, Heze, 274000, Shandong, China.
Yujie MaDepartment of Infectious Diseases, Heze Municipal Hospital, No2888 Caozhou Road, Heze, 274000, Shandong, China.
Aiying ZhaoDepartment of Infectious Diseases, Heze Municipal Hospital, No2888 Caozhou Road, Heze, 274000, Shandong, China. zhaoaiying0022@sina.com.ORCID http://orcid.org/0000-0001-7123-4478
Heze Municipal Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis has become a major social, health, and economic problem worldwide. Herein, we tested the beneficial influence of baicalin, a flavonoid extracted from the roots of Scutellaria baicalensis, on human normal liver L-02 and THLE2 cell apoptosis and inflammatory reaction stimulated by lipopolysaccharide (LPS) and possible molecular mechanisms. L-02 and THLE2 cell viability and apoptosis after LPS and/or baicalin treatment were tested using CCK-8 assay and Annexin V-FITC/PI apoptosis kit, respectively. qRT-PCR was used to measure the MCP-1, IL-6, TNF-α, and lncRNA taurine upregulated gene 1 (TUG1) expressions in L-02 and THLE2 cells. sh-TUG1 was transfected to knockdown TUG1. SB203580 was used as inhibitor of p38MAPK pathway, while SP600125 was used as inhibitor of JNK pathway. We discovered that LPS stimulation caused L-02 and THLE2 cell apoptosis and inflammatory reaction. Baicalin relieved the L-02 and THLE2 cell apoptosis and inflammatory reaction stimulated by LPS. Moreover, LPS lowered the TUG1 expression in L-02 cells, while baicalin promoted the TUG1 expression in L-02 and L-02 and THLE2 cells, as well as inactivated p38MAPK and JNK pathways in LPS-stimulated L-02 cells. Besides, knockdown of TUG1 activated p38MAPK and JNK pathways and promoted inflammatory cytokine expression in L-02 cells. In conclusion, this study further affirmed the beneficial influences of baicalin on LPS-stimulated human normal liver cell apoptosis and inflammatory reaction. Baicalin relived liver cell inflammation stimulated by LPS might be via upregulating TUG1 and then inactivating p38MAPK and JNK pathways.

Indexed as

Anti-Inflammatory Agents, Non-SteroidalApoptosisCell LineFlavonoidsHepatitisHepatocytesHumansInflammationLipopolysaccharidesLiverMAP Kinase Kinase 4p38 Mitogen-Activated Protein KinasesRNA, Long NoncodingScutellaria baicalensisAnti-Inflammatory Agents, Non-SteroidalbaicalinFlavonoidsLipopolysaccharidesMAP Kinase Kinase 4p38 Mitogen-Activated Protein KinasesRNA, Long NoncodingTUG1 long noncoding RNA, humanBaicalinHepatitisJNK pathwayLipopolysaccharideLncRNA TUG1p38MAPK pathway

Identifiers

PMID31396818
OpenAlexW2967634567

What OpenQuestion 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 OpenQuestion graph.