Evidence map›Paper›PMID 32683581›Full record

ArticleCellular and molecular neurobiology2021

SIRT1 Activation by Polydatin Alleviates Oxidative Damage and Elevates Mitochondrial Biogenesis in Experimental Diabetic Neuropathy.

Preethi Bheereddy, Veera Ganesh Yerra, Anil Kumar Kalvala, Bhoomika Sherkhane, Ashutosh Kumar

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 73 citations in OpenAlex.

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  15. Pharmaceuticals (Basel, Switzerland) · 2024
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  17. Article
  18. Applications of Cannabinoids in Neuropathic Pain: An Updated Review.Critical reviews in therapeutic drug carrier systems · 2024
    Review
  19. Article
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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

5 authors at 3 institutions in 2 countries.

Preethi BheereddyDepartment of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Balanagar, Hyderabad, 500037, India.
Veera Ganesh YerraSt. Michael's Hospital, Keenan Research Centre for Biomedical Science and Li Ka Shing Knowledge Institute, Toronto, ON, Canada.
Anil Kumar KalvalaDepartment of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Balanagar, Hyderabad, 500037, India.
Bhoomika SherkhaneDepartment of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Balanagar, Hyderabad, 500037, India.
Ashutosh KumarDepartment of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Balanagar, Hyderabad, 500037, India. drashutoshniper@gmail.com.ORCID http://orcid.org/0000-0001-6659-4751
National Institute of Pharmaceutical Education and Research · INNational Institute of Pharmaceutical Education and Research (NIPER) - Ahmedabad · INSt. Michael's Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction has been implicated as a one of the major factors linked to the development of painful diabetic neuropathy (DN). Several studies have demonstrated that sirtuin (SIRT1) activation recuperates nerve function by activating mitochondrial biogenesis. Polydatin, a resveratrol glycoside, has been explored to improve mitochondrial function via SIRT1 activation. However, the neuroprotective effects of polydatin in DN remain elusive. In this study, polydatin (25 and 50 mg/kg, oral) was administered for last 2 weeks of 8-week study to diabetic Sprague-Dawley rats weighing 250-300 g (post 6-weeks of streptozotocin 55 mg/kg, intraperitoneal). Treatment with polydatin significantly attenuated mechanical and thermal hyperalgesia in diabetic rats. Treated diabetic rats also showed improvement in motor/sensory nerve conduction velocities and nerve blood flow. For in vitro studies, Neuro2a cells were exposed to high-glucose (30 mM) condition to simulate short-term hyperglycemia. Polydatin was evaluated for its role in SIRT1 and Nrf2 activation at a dose of 5, 10, and 20 µM concentrations. Polydatin exposure normalized the mitochondrial superoxides, membrane potentials and improved neurite outgrowth in high-glucose-exposed Neuro2a cells. Increased SIRT1 activation by polydatin resulted in peroxisome proliferator activated receptor-gamma coactivator-1α (PGC-1α) directed mitochondrial biogenesis. SIRT1 activation also facilitated Nrf2-directed antioxidant signaling. Study results inferred that decline in mitochondrial biogenesis and oxidative function in diabetic rats and high-glucose-exposed Neuro2a cells, could be counteracted by polydatin administration, postulated via enhancing SIRT1 and Nrf2 axis.

Indexed as

AnimalsAntioxidantsDiabetes Mellitus, ExperimentalDiabetic NeuropathiesGlucosidesMiceMitochondriaOrganelle BiogenesisOxidative StressSirtuin 1StilbenesStreptozocinAntioxidantsGlucosidespolydatinSirt1 protein, ratSirtuin 1StilbenesStreptozocinMitochondrial biogenesisNrf2Oxidative stressPolydatinSIRT1

Identifiers

PMID32683581
PMCPMC11448605
OpenAlexW3042639872

What OpenQuestion holds

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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.