ArticleInflammation2026
Carnosic Acid Protects against Bisphenol A-Induced NLRP3 Inflammasome Activation by Attenuating Oxidative Stress in Human Microglial Cells.
Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Bisphenol A (BPA) is an endocrine-disrupting chemical commonly found in consumer products and is known to induce neuroinflammation and oxidative stress via microglial activation. Carnosic acid (CA), a phenolic diterpene from rosemary (Rosmarinus officinalis L.), has potent antioxidant and neuroprotective properties. This study investigated the protective effects of CA against BPA-induced neuroinflammation and oxidative stress in human HMC3 microglial cells. Firstly, BPA induced the expression of NLRP3 inflammasome–related proteins and increased NLRP3 fluorescence intensity. CA reduced the fluorescence intensity of NLRP3 and cleaved caspase-1 induced by BPA. CA also attenuated BPA-induced protein levels in the inflammasome, proinflammatory cytokines, and phosphorylated tau, as well as the transcription factors FoxO1 and p65. CA improved the effects in BPA-induced ROS level and reduced the expression of catalase, glutathione reductase, superoxide dismutase 2 (SOD2), glutathione peroxidase 1, heme oxygenase-1, nuclear factor erythroid 2-related factor 2 (Nrf2), and UDP-glucuronosyltransferase 1A1 (UGT1A1). In addition, CA restored BPA-suppressed expression of UGT1A1 and SOD2 in the striatum of mice. L-Buthionine-sulfoximine (BSO) treatment abolished CA’s ability to counteract BPA-induced oxidative stress and inflammatory responses. These findings indicated that CA was associated with attenuation of BPA-induced NLRP3 inflammasome-related protein expression and downstream neuroinflammatory signaling by reducing oxidative stress in HMC3 cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.