Evidence map›Paper›PMID 40358918›Full record

ArticleCell biochemistry and biophysics2025

Micronized Purified Flavonoid Fraction (Diosmin/Hesperidin) Ameliorates Cardiac Structural and Functional Integrity in Cisplatin-treated Male Wistar Rats by Modulating NLRP3/Caspase-1/-3 Signaling.

W A Saka, P A Oyedokun, C A Adegbola, T M Akhigbe, P J Ashonibare, O R Kolawole, A A Oladipo, R E Akhigbe

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Article in Cell biochemistry and biophysics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
4 · The record

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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.

W A SakaDepartment of Physiology, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
P A OyedokunDepartment of Physiology, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
C A AdegbolaDepartment of Physiology, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
T M AkhigbeReproductive Biology and Toxicology Research Laboratory, Oasis of Grace Hospital, Osogbo, Osun State, Nigeria.
P J AshonibareDepartment of Physiology, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
O R KolawoleDepartment of Physiology, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
A A OladipoDepartment of Physiology, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
R E AkhigbeDepartment of Physiology, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria. reakhigbe@lautech.edu.ng.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin is an effective chemotherapeutic agent in managing several cancers. Yet, its usage is restricted by its toxicity to non-target organs, such as cardiotoxicity that is mediated by nucleotide-binding Oligomerisation Domain (NOD)-Like Receptors family pyrin domain containing 3 (NLRP3)-driven inflammation, oxidative stress, and apoptosis. Conversely, micronized purified flavonoid fractions (MPFF) attenuate oxido-inflammation by downregulating NLRP3 inflammasome. However, there is a dearth of information on the effect of MPFF on cisplatin-induced cardiac injury. This study examined the possible protective effect of MPFF in cisplatin-induced cardiac injury. Also, the role of NLRP3 inflammasome and caspase-1/-3 signaling was evaluated. Thirty-two adult male Wistar rats were randomly allotted to four equal groups (n = 8 rats per group). The control received 0.5 mL of distilled water orally daily, the MPFF-treated rats received 100 mg/kg/day of MPFF orally for 14 days, the cisplatin-treated rats had 7 mg/kg of cisplatin via an intraperitoneal route on day 8, and the cisplatin+MPFF -treated rats received cisplatin and MPFF as those in the cisplatin- and MPFF-treated groups. Cisplatin therapy significantly increased cardiac injury markers and plasma glucose. Cisplatin also induced dyslipidemia and insulin resistance. Moreover, cisplatin altered cardiac histology evidenced by vascular congestion, and increased myofibril thickness and interstitial space. These observations were accompanied by cisplatin-induced cardiac oxidative stress (increased malondialdehyde and a decline in reduced glutathione, superoxide dismutase, and catalase), inflammation (increased tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6), apoptosis (increased caspase 1 and caspase 3) and a marked increase in NLPR3 inflammasome. These derangements were blunted by MPFF co-therapy. In conclusion, this study for the first time demonstrated that MPFF attenuated cisplatin-induced cardiac structural and functional damage by suppressing oxidative stress and inflammation via the downregulation of NLPR3 /caspase-1/-3 signaling.

Indexed as

CisplatinDiosminFlavonoidsHeartHesperidinNLR Family, Pyrin Domain-Containing 3 ProteinSignal TransductionAnimalsAntineoplastic AgentsCaspase 1InflammasomesMaleMyocardiumOxidative StressRatsRats, WistarAntineoplastic AgentsCaspase 1CisplatinDiosminFlavonoidsHesperidinInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratAntioxidantApoptosisChemotherapyFlavonoidInflammationOxidative stress

Identifiers

PMID40358918

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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.