Evidence map›Paper›PMID 41451364›Full record

ArticleFrontiers in pharmacology2025

Isoliensinine confers neuroprotection and alleviates LPS-induced neuroinflammation in microglia by regulating the MAPK/NF-κB signaling.

Mengqin Yuan, Jinda Hu, Lichen Gao, Wei Long, Sirui Wang, Xinyue Tan, Jinyue Hu

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

7 authors.

Mengqin YuanDepartment of Pharmacy, School of Pharmaceutical Science, Phase I Clinical Trial Centre, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Jinda HuDepartment of Pharmacy, School of Pharmaceutical Science, Phase I Clinical Trial Centre, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Lichen GaoDepartment of Pharmacy, School of Pharmaceutical Science, Phase I Clinical Trial Centre, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Wei LongDepartment of Pharmacy, School of Pharmaceutical Science, Phase I Clinical Trial Centre, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Sirui WangDepartment of Pharmacy, School of Pharmaceutical Science, Phase I Clinical Trial Centre, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Xinyue TanSchool of Life Science, Hunan University of Science and Technology, Xiangtan, China.
Jinyue HuMedical Research Center, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The increasing aged population poses issues in the management of age-related disorders, notably Alzheimer's disease (AD), which significantly affects the health and quality of life of seniors. Neuroinflammation is a significant factor in Alzheimer's disease pathogenesis. Isoliensinine (ISO), a bisbenzylisoquinoline alkaloid derived from lotus seed embryos, exhibits antioxidant and anti-inflammatory effects. Nonetheless, its function in neuroinflammation has yet to be investigated. Methods: We examined the impact of ISO on LPS-induced neuroinflammation in BV2 microglial cells by using biological tests. Western blotting confirmed ISO's influence on MAPK/NF-κB signaling pathways. In addition, oxidative stress markers and JC-1 staining were employed to assess the impact of ISO on LPS-induced oxidative stress and mitochondrial dysfunction in BV2 cells. Results: ISO markedly diminished LPS-induced neuroinflammation in BV2 cells through the modulation of the MAPK/NF-κB pathway. Conditioned media derived from ISO-treated BV2 cells enhanced the vitality of HT-22 cells. ISO also alleviated oxidative stress and mitochondrial dysfunction. Conclusion: Our findings indicate that ISO mitigates neuroinflammation by inhibiting MAPK/NF-κB signaling and provides neuroprotection by diminishing oxidative stress and mitochondrial impairment. These effects collectively enhance its neuroprotective capacity, indicating that ISO may represent a potential candidate for further investigation in AD.

Indexed as

Alzheimer’s diseaseisoliensinineLPSMAPK/NF-κBneuroinflammationneuroprotection

Identifiers

PMID41451364
PMCPMC12727965

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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.