Evidence map›Paper›PMID 28181071›Full record

ArticleNeurochemical research2017

Neurotrophic Effect of Asiatic acid, a Triterpene of Centella asiatica Against Chronic 1-Methyl 4-Phenyl 1, 2, 3, 6-Tetrahydropyridine Hydrochloride/Probenecid Mouse Model of Parkinson's disease: The Role of MAPK, PI3K-Akt-GSK3β and mTOR Signalling Pathways.

Jagatheesan Nataraj, Thamilarasan Manivasagam, Arokiasamy Justin Thenmozhi, Musthafa Mohamed Essa

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.7field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Neurotrophic Natural Products.Progress in the chemistry of organic natural products · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Multi-Target Approach ofPharmaceuticals (Basel, Switzerland) · 2022
    Review
  16. Terpenoid natural products exert neuroprotectionFrontiers in pharmacology · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 2 institutions in 2 countries.

Jagatheesan NatarajDepartment of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, Tamilnadu, 608002, India.
Thamilarasan ManivasagamDepartment of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, Tamilnadu, 608002, India. mani_pdresearchlab@rediffmail.com.
Arokiasamy Justin ThenmozhiDepartment of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, Tamilnadu, 608002, India.
Musthafa Mohamed EssaDepartment of Food Science and Nutrition, CAMS, Sultan Qaboos University, Muscat, Oman.
Annamalai University · INIndia Diabetes Research Foundation · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulation of various signalling (Ras-MAPK, PI3K and AKT) pathways by augmented activity of neurotrophic factors (NTFs) could prevent or halt the progress of dopaminergic loss in Parkinson's disease (PD). Various in vitro and in vivo experimental studies indicated anti-parkinsonic potential of asiatic acid (AA), a pentacyclic triterpene obtained from Centella asiatica. So the present study is designed to determine the neurotrophic effect of AA against 1-methyl 4-phenyl 1, 2, 3, 6-tetrahydropyridine hydrochloride/probenecid (MPTP/p) neurotoxicity in mice model of PD. AA treatment for 5 weeks significantly attenuated MPTP/p induced motor abnormalities, dopamine depletion and diminished expressions NTFs and tyrosine kinase receptors (TrKB). We further, revealed that AA treatment significantly inhibited the MPTP/p-induced phosphorylation of MAPK/P38 related proteins such as JNK and ERK. Moreover, AA treatment increased the phosphorylation of PI3K, Akt, GSK-3β and mTOR, suggesting that AA activated PI3K/Akt/mTOR signalling pathway, which might be the cause of neuroprotection offered by AA. The present findings provided more elaborate in vivo evidences to support the neuroprotective effect of AA on dopaminergic neurons of chronic Parkinson's disease mouse model and the potential of AA to be developed as a possible new therapeutic target to treat PD.

Indexed as

AnimalsGlycogen Synthase Kinase 3 betaMaleMiceMice, Inbred C57BLMitogen-Activated Protein Kinase KinasesMPTP PoisoningNeuroprotective AgentsOncogene Protein v-aktPentacyclic TriterpenesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProbenecidTOR Serine-Threonine KinasesTreatment Outcomeasiatic acidGlycogen Synthase Kinase 3 betaMitogen-Activated Protein Kinase KinasesmTOR protein, mouseNeuroprotective AgentsOncogene Protein v-aktPentacyclic TriterpenesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProbenecidTOR Serine-Threonine KinasesApoptosisAsiatic acidMPTP/pNTFsParkinson’s diseasePI3K/Akt

Identifiers

PMID28181071
OpenAlexW2586654463

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.