Evidence map›Paper›PMID 42405401›Full record

ReviewCurrent pharmaceutical design2026

Resveratrol and the NLRP3 Inflammasome: Unlocking the Anti-inflammatory Potential of a Natural Compound.

Komal Sharma, Neelam Singla, Satvinder Kaur, Meenakshi Bhatkatiya, Rajat Vaisnav, Rupesh Kumar Gautam, Srishti Gautam, Havagiray Chitme

Abstract readReview
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In one paragraph

Review in Current pharmaceutical design, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Komal SharmaBhupal Noble's Institute of Pharmaceutical Sciences, Udaipur, Rajasthan, India.
Neelam SinglaDepartment of Pharmacy, Suresh Gyan Vihar University, Jaipur, Rajasthan, India.
Satvinder KaurGHG Khalsa College of Pharmacy, Gurusar Sadhar, Ludhiana, Punjab, India.
Meenakshi BhatkatiyaBhupal Noble's Institute of Pharmaceutical Sciences, Udaipur, Rajasthan, India.
Rajat VaisnavBhupal Noble's Institute of Pharmaceutical Sciences, Udaipur, Rajasthan, India.
Rupesh Kumar GautamAmity Institute of Pharmacy, Amity University Uttar Pradesh, Noida, India.
Srishti GautamSree Uthradom Thirunal Academy of Medical Sciences, Department of Paediatrics, Vattapara, Thiruvananthapuram, Kerala, India.
Havagiray ChitmeAmity Institute of Pharmacy, Amity University Uttar Pradesh, Noida, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

INTRODUCTION/

objectiveChronic inflammation is the basis of various diseases, including inflammatory bowel disease, neurodegenerative diseases, and cardiometabolic disorders. NLRP3 is a key player in controlling Interleukin-1β (IL-1β) and Interleukin-18 (IL-18) maturation and pyroptosis via its NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome. This review will assess the mechanistic and therapeutic opportunity of resveratrol in restraining the NLRP3 inflammasome activation.

methodsA search of experimental and preclinical studies examining the impact of resveratrol on oxidative stress, inflammatory signaling, mitochondrial activity, and inflammasome activation in various disease models was performed.

resultsResveratrol reduces oxidative stress by regulating reactive oxygen species-mediated nuclear factor erythroid 2-related factor 2 signaling and suppressing toll-like receptor 4 (TLR4) /nuclear factor kappa B signaling (NF-κB). It maintains mitochondrial integrity by activating sirtuin 1 and AMP-activated protein kinase signalling. In models of acute lung injury, bronchitis, diabetic nephropathy, and neurodegeneration, resveratrol can suppress the expression of NLRP3, caspase-1, and IL-1β, promote autophagy, and prevent dopaminergic neurons through the PINK1/Parkin/NLRP3 pathway. Additionally, it enhances intestinal barrier integrity in dextran sulfate sodium-induced colitis and suppresses inflammasome-mediated inflammation. DISCUSSION: These results suggest that resveratrol regulates the priming and activation stages of NLRP3 inflammasome signaling by inhibiting oxidative stress, mitochondrial dysfunction, and inflammatory cascades based on redox signaling. Nanoparticle preparations and structural analogs, such as pterostilbene, improve stability, bioavailability, and specific delivery.

conclusionResveratrol is a potential natural therapeutic agent for managing NLRP3 inflammasomemediated inflammation, and its efficacy is enhanced when administered in optimal formulations and combined with conventional anti-inflammatory agents.

Indexed as

Anti-Inflammatory AgentsAnti-Inflammatory Agents, Non-SteroidalBiological ProductsInflammasomesInflammationNLR Family, Pyrin Domain-Containing 3 ProteinResveratrolAnimalsHumansOxidative StressAnti-Inflammatory AgentsAnti-Inflammatory Agents, Non-SteroidalBiological ProductsInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinResveratrolautophagyinflammasomesmitochondriaNLRP3 inflammasomeoxidative stresspyroptosisreactive oxygen speciesResveratrol

Identifiers

What Socratic 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 Socratic graph.