Evidence map›Paper›PMID 38329438›Full record

ArticleAging2024

Minocycline alleviates LPS-induced cognitive dysfunction in mice by inhibiting the NLRP3/caspase-1 pathway.

Fenfang Zhan, Yao Dong, Lanqian Zhou, Xiaozhong Li, Zheng Zhou, Guohai Xu

Abstract read
In one paragraph

Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Minocycline-containing therapy inTherapeutic advances in gastroenterology · 2026
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Gut-Brain Axis: Focus on Sex Differences in Neuroinflammation.International journal of molecular sciences · 2024
    Review
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

6 authors.

Fenfang ZhanDepartment of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Yao DongDepartment of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Lanqian ZhouDepartment of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Xiaozhong LiDepartment of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Zheng ZhouDepartment of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Guohai XuDepartment of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGrowing experimental evidence indicates that cognitive impairment is linked to neuroinflammation. Minocycline (MINO), an antibiotic known for its anti-inflammatory, has shown promise in alleviating cognitive impairment. Nonetheless, the exact mechanism through which MINO improves cognitive impairment is not yet understood.

methodsA neuroinflammatory model was establish by utilizing lipopolysaccharide. The assessment of mice's cognitive and learning abilities was conducted through the MWM and Y-maze tests. The evaluation of hippocampal neuronal injury and microglial activation were achieved by performing HE staining and IHC, respectively. To evaluate BV2 cell viability and apoptosis, the CCK-8 and Hoechst 33342/PI staining assays were employed. In order to assess the protein and RNA expression levels of NLRP3, caspase-1, IL-1β, IL-18, Iba-1, and Bcl2/Bax, WB and RT-qPCR were utilized. Additionally, the inhibitory effect of MINO on apoptosis by targeting the NLRP3/caspase-1 pathway was investigated using Nigericin.

resultsMINO was effective in reducing the time it took for mice to escape from the test, increasing the number of platforms they crossed, and mitigating damage to the hippocampus while also suppressing microglial activation and the expression of Iba-1 in a neuroinflammatory model caused by LPS. Furthermore, MINO improved the viability of BV2 cell and reduced apoptosis. It also had the effect of reducing the expression levels of NLRP3/Caspase-1, IL-1β, IL-18, and BAX, while upregulating the expression of Bcl2. Additionally, MINO was found to downregulate the NLRP3 expression, which is specifically activated by nigericin.

conclusionThe protective effect of MINO relies on the crucial involvement of the NLRP3/caspase-1 pathway.

Indexed as

Cognitive DysfunctionNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsbcl-2-Associated X ProteinCaspase 1Interleukin-18LipopolysaccharidesMiceMinocyclineNigericinbcl-2-Associated X ProteinCaspase 1Interleukin-18LipopolysaccharidesMinocyclineNigericinNLR Family, Pyrin Domain-Containing 3 Proteincaspase-1cognitive dysfunctionlipopolysaccharideminocyclineNOD-like receptor protein-3

Identifiers

PMID38329438
PMCPMC10911373

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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.