Evidence map›Paper›PMID 35408478›Full record

ArticleMolecules (Basel, Switzerland)2022

Neuroprotective Effects of Green Tea Seed Isolated Saponin Due to the Amelioration of Tauopathy and Alleviation of Neuroinflammation: A Therapeutic Approach to Alzheimer's Disease.

Muhammad Imran Khan, Muhammad Zubair Khan, Jin Hyuk Shin, Tai Sun Shin, Young Bok Lee, Min Yong Kim, Jong Deog Kim

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 19 citations in OpenAlex.

  1. Unlocking the Neuroprotective Potential ofAntioxidants (Basel, Switzerland) · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Therapeutic Candidates for Alzheimer's Disease: Saponins.International journal of molecular sciences · 2023
    Review
  8. Review
  9. 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

7 authors at 1 institution in 1 country.

Muhammad Imran KhanDepartment of Biotechnology, Chonnam Notational University, Chonnam, Yeosu 59626, Korea.ORCID 0000-0003-1096-1529
Muhammad Zubair KhanDepartment of Biotechnology, Chonnam Notational University, Chonnam, Yeosu 59626, Korea.
Jin Hyuk ShinDepartment of Biotechnology, Chonnam Notational University, Chonnam, Yeosu 59626, Korea.
Tai Sun ShinDepartment of Food Science and Nutrition, Chonnam National University, Gwangju 61186, Korea.
Young Bok LeeDepartment of Refrigeration Engineering, Chonnam National University Yeosu, Chonnam 59626, Korea.
Min Yong KimResearch Center on Anti-Obesity and Health Care, Chonnam National University, Chonnam, Yeosu 59626, Korea.
Jong Deog KimDepartment of Biotechnology, Chonnam Notational University, Chonnam, Yeosu 59626, Korea.
Chonnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tauopathy is one of the major causes of neurodegenerative disorders and diseases such as Alzheimer's disease (AD). Hyperphosphorylation of tau proteins by various kinases leads to the formation of PHF and NFT and eventually results in tauopathy and AD; similarly, neuroinflammation also exaggerates and accelerates neuropathy and neurodegeneration. Natural products with anti-tauopathy and anti-neuroinflammatory effects are highly recommended as safe and feasible ways of preventing and /or treating neurodegenerative diseases, including AD. In the present study, we isolated theasaponin E1 from ethanol extract of green tea seed and evaluated its therapeutic inhibitory effects on tau hyper-phosphorylation and neuroinflammation in neuroblastoma (SHY-5Y) and glioblastoma (HTB2) cells, respectively, to elucidate the mechanism of the inhibitory effects. The expression of tau-generating and phosphorylation-promoting genes under the effects of theasaponin E1 were determined and assessed by RT- PCR, ELISA, and western blotting. It was found that theasaponin E1 reduced hyperphosphorylation of tau and Aβ concentrations significantly, and dose-dependently, by suppressing the expression of GSK3 β, CDK5, CAMII, MAPK, EPOE4(E4), and PICALM, and enhanced the expression of PP1, PP2A, and TREM2. According to the ELISA and western blotting results, the levels of APP, Aβ, and p-tau were reduced by treatment with theasaponin E1. Moreover, theasaponin E1 reduced inflammation by suppressing the Nf-kB pathway and dose-dependently reducing the levels of inflammatory cytokines such as IL-1beta, IL-6, and TNF-alpha etc.

Indexed as

Alzheimer DiseaseNeuroprotective AgentsSaponinsGlycogen Synthase Kinase 3HumansNeuroinflammatory DiseasesPhosphorylationSeedstau ProteinsTeaGlycogen Synthase Kinase 3Neuroprotective AgentsSaponinstau ProteinsTeakinasesneurodegenerationneurofibrillary tanglesneuroinflammationSHY-5Y cellstaupathy

Identifiers

PMID35408478
PMCPMC9000224
OpenAlexW4220852146

What OpenQuestion holds

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LicenceCC BY
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.