Evidence map›Paper›PMID 36577854›Full record

ArticleTranslational stroke research2024

A Novel Hybrid of Telmisartan and Borneol Ameliorates Neuroinflammation and White Matter Injury in Ischemic Stroke Through ATF3/CH25H Axis.

Xin Guan, Jianbing Wu, Jiahui Geng, Duorui Ji, Dasha Wei, Yong Ling, Yihua Zhang, Guojun Jiang, Tao Pang, Zhangjian Huang

Abstract read
PubMed Publisher
In one paragraph

Article in Translational stroke research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
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

10 authors at 5 institutions in 1 country.

Xin Guan *State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Drug Discovery for Metabolic Diseases, Center of Drug Discovery, New Drug Screening Center, Jiangsu Center for Pharmacodynamics Research and Evaluation, Institute of Pharmaceutical Sciences, China Pharmaceutical University, #24 Tong Jia Xiang Street, Nanjing, 210009, People's Republic of China.
Jianbing Wu *State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Drug Discovery for Metabolic Diseases, Center of Drug Discovery, New Drug Screening Center, Jiangsu Center for Pharmacodynamics Research and Evaluation, Institute of Pharmaceutical Sciences, China Pharmaceutical University, #24 Tong Jia Xiang Street, Nanjing, 210009, People's Republic of China.
Jiahui GengState Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Drug Discovery for Metabolic Diseases, Center of Drug Discovery, New Drug Screening Center, Jiangsu Center for Pharmacodynamics Research and Evaluation, Institute of Pharmaceutical Sciences, China Pharmaceutical University, #24 Tong Jia Xiang Street, Nanjing, 210009, People's Republic of China.
Duorui JiState Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Drug Discovery for Metabolic Diseases, Center of Drug Discovery, New Drug Screening Center, Jiangsu Center for Pharmacodynamics Research and Evaluation, Institute of Pharmaceutical Sciences, China Pharmaceutical University, #24 Tong Jia Xiang Street, Nanjing, 210009, People's Republic of China.
Dasha WeiState Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Drug Discovery for Metabolic Diseases, Center of Drug Discovery, New Drug Screening Center, Jiangsu Center for Pharmacodynamics Research and Evaluation, Institute of Pharmaceutical Sciences, China Pharmaceutical University, #24 Tong Jia Xiang Street, Nanjing, 210009, People's Republic of China.
Yong LingSchool of Pharmacy, Nantong University, Nantong, 226001, People's Republic of China.
Yihua ZhangState Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Drug Discovery for Metabolic Diseases, Center of Drug Discovery, New Drug Screening Center, Jiangsu Center for Pharmacodynamics Research and Evaluation, Institute of Pharmaceutical Sciences, China Pharmaceutical University, #24 Tong Jia Xiang Street, Nanjing, 210009, People's Republic of China.
Guojun JiangDepartment of Pharmacy, Zhejiang Xiaoshan Hospital, Hangzhou, 311201, People's Republic of China.
Tao PangState Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Drug Discovery for Metabolic Diseases, Center of Drug Discovery, New Drug Screening Center, Jiangsu Center for Pharmacodynamics Research and Evaluation, Institute of Pharmaceutical Sciences, China Pharmaceutical University, #24 Tong Jia Xiang Street, Nanjing, 210009, People's Republic of China. tpang@cpu.edu.cn.
Zhangjian HuangState Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Drug Discovery for Metabolic Diseases, Center of Drug Discovery, New Drug Screening Center, Jiangsu Center for Pharmacodynamics Research and Evaluation, Institute of Pharmaceutical Sciences, China Pharmaceutical University, #24 Tong Jia Xiang Street, Nanjing, 210009, People's Republic of China. zhangjianhuang@cpu.edu.cn.
State Key Laboratory of Natural MedicineChina Pharmaceutical University · CNNanjing University · CNNantong University · CNThe First People's Hospital of Xiaoshan District, Hangzhou · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral ischemic stroke causes substantial white matter injury, which is further aggravated by neuroinflammation mediated by microglia/astrocytes. Given the anti-neuroinflammatory action of telmisartan and the enhancing blood-brain barrier (BBB) permeability potential of resuscitation-inducing aromatic herbs, 13 hybrids (3a-m) of telmisartan (or its simplified analogues) with resuscitation-inducing aromatic agents were designed, synthesized, and biologically evaluated. Among them, the optimal compound 3a (the ester hybrid of telmisartan and (+)-borneol) potently inhibited neuroinflammation mediated by microglia/astrocytes and ameliorated ischemic stroke. Particularly, 3a significantly conferred protection for white matter integrity after cerebral ischemic stroke via decreasing abnormally dephosphorylated neurofilament protein, upregulating myelin basic protein, and attenuating oligodendrocyte damage. Further RNA-sequencing data revealed that 3a upregulated expression of transcriptional regulator ATF3 to reduce the expression of CH25H, prevented proinflammatory state of lipid-droplet-accumulating microglia/astrocytes to limit excessive inflammation, and eventually protected neighboring oligodendrocytes to prevent white matter injury. Taken with the desirable pharmacokinetics behavior and improved brain distribution, 3a may be a feasible therapeutic agent for ischemic stroke and other neurological disorders with white matter injury.

Indexed as

Brain InjuriesCamphanesIschemic StrokeStrokeWhite MatterActivating Transcription Factor 3HumansMicrogliaNeuroinflammatory DiseasesTelmisartanActivating Transcription Factor 3ATF3 protein, humanCamphanesisoborneolTelmisartanATF3BorneolIschemic strokeNeuroinflammationTelmisartanWhite matter injury

Identifiers

PMID36577854
OpenAlexW4313231626

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.