ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
Targeting inflammatory dysregulation in metabolic dysfunction-associated steatotic liver disease rat model: the preventive and therapeutic effects of acetyl-11-keto-beta-boswellic acid.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. 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
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic associated fatty liver disease (MASLD) is a global health issue affecting over 30% of the population and can progress to severe liver conditions such as cirrhosis and hepatocellular carcinoma (HCC). The progression of MASLD is driven by underlying metabolic dysregulation and chronic inflammation. This study aims to evaluate the therapeutic efficacy of acetyl-11-keto-β-boswellic acid (AKBA) in a rat model of MASLD induced by a high-fat and high-fructose diet (HFrD). We hypothesize that AKBA supplementation will suppress pro-inflammatory cytokine expression and inhibit inflammatory signaling pathways, thereby ameliorating MASLD progression. MASLD was induced in 36 male rats, randomly divided into two main groups: prevention (6-week regimen) and treatment (8-week regimen). Each group was further divided into three subgroups: Control, HFrD, and AKBA. In the prevention group, the subgroup receiving a high-fat, high-fructose diet (HFrD) was simultaneously administered AKBA. In the treatment group, after inducing MASLD with HFrD, AKBA was administered as a therapeutic intervention. Serum levels of IL-2, pro-inflammatory cytokines (IL-1β, IL-18, IL-1α), and anti-inflammatory cytokines (IL-1Ra, IL-10) were measured using ELISA. Additionally, IL-1R1 gene expression was analyzed using quantitative real-time PCR. Histological examinations of liver tissues were conducted to assess triglyceride accumulation. AKBA significantly reduced serum levels of pro-inflammatory cytokines, including IL-1α, IL-1β, and IL-18, which are key products of the NLRP3 inflammasome complex, as well as reduced IL-2 serum levels. It also increased levels of the anti-inflammatory cytokines IL-1Ra and IL-10. Additionally, AKBA mitigated weight gain and decreased triglyceride accumulation in liver tissues compared to the HFrD group. AKBA exhibits potent anti-inflammatory properties that ameliorate MASLD by reducing hepatic steatosis and inflammatory markers. Further studies, including extended durations and human clinical trials, are warranted to fully elucidate AKBA's therapeutic potential.
Indexed as
Identifiers
40478334What Socratic 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 Socratic graph.