In this study, we sought to evaluate changes in peritumoral fibrosis after transarterial chemoembolization (TACE) in a rabbit VX2 liver tumor model using intravoxel incoherent motion diffusion-weighted imaging (IVIM DWI) and ultrasound shear wave elastography (SWE). A total of 20 rabbits underwent implantation of VX2 tumor tissues in the left lobe of the liver. The rabbits were randomly divided into an experimental group ( = 10) or a control group ( = 10). Those in the experimental group were treated with an emulsion of lipiodol and pirarubicin through a microcatheter 2-3 weeks after implantation; those in the control group were treated with sterile water. Compared with the control group, the true diffusion coefficient (D) and pseudodiffusion coefficient (D*) values in liver tissues were significantly lower (p < 0.05 for all) and liver stiffness values (LSV) (10.58 ± 0.89 kPa) were higher in the experimental group (7.65 ± 0.86 kPa; p < 0.001). The median stage of liver fibrosis based on METAVIR scores was 1 (1,1) in the control group and 2 (2,3) in the experimental group ( = 4.15, p < 0.001). D, D*, and LSV were significantly correlated with pathologic staining in the assessment of liver fibrosis ( = -0.54 p = 0.015; = -0.50, p = 0.025; = 0.91, p < 0.001; respectively). These data suggest that TACE aggravates liver injury and liver fibrosis, especially surrounding the tumor, in a rabbit VX2 liver tumor model. IVIM DWI and SWE can be used to evaluate the change in liver fibrosis.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9597251 | PMC |
| http://dx.doi.org/10.3389/fphys.2022.893925 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Predictive value of neutrophil-to-lymphocyte ratio and MELD score for short-term survival of patients with HBV-DeCi.
Biomark Med
January 2025
Department of Laboratory Medicine, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Objective: The prognostic value of neutrophil-to-lymphocyte ratio (NLR) combined with Model for End-Stage Liver Disease (MELD) score was evaluated for hepatitis B virus-associated decompensated cirrhosis (HBV-DeCi).
Methods: The 30-day mortality of 166 hBV-DeCi patients was examined. Receiver operating characteristic curve analysis and multivariate regression analysis were used to assess the performance of NLR for prediction of poor outcomes.
Tubulointerstitial nephritis antigen-like 1 promotes the progression of liver fibrosis after HCV eradication with direct-acting antivirals.
Int J Biol Sci
January 2025
CAMS Key Laboratory of Antiviral Drug Research, Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100050, China.
Although therapies based on direct-acting antivirals (DAAs) effectively eradicate hepatitis C virus (HCV) in patients, there is still a high risk of liver fibrosis even after a sustained virological response. Therefore, it is of great clinical importance to understand the mechanism of potential factors that promote liver fibrosis after virological cure by treatment with DAAs. Here, we found that tubulointerstitial nephritis antigen-like 1 (TINAGL1) is significantly increased in HCV-infected hepatocytes and in the liver of patients with liver fibrosis, and that higher TINAGL1 expression persists in HCV-eradicated hepatocytes after treatment with DAAs.
View Article and Find Full Text PDFCaveolin-1 mitigates the advancement of metabolic dysfunction-associated steatotic liver disease by reducing endoplasmic reticulum stress and pyroptosis through the restoration of cholesterol homeostasis.
Int J Biol Sci
January 2025
Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, China.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease worldwide, which has the potential to advance to fibrosis. CAV1 has the effects of improving liver lipid deposition in MASLD, however, the potential mechanism is largely unknown. Here, we establish a MASLD mouse model in CAV1 knockout (KO) mice and perform transcriptome analysis on livers from mice to investigate the effects of CAV1 in MASLD progression.
View Article and Find Full Text PDFUSP25 stabilizes STAT6 to promote IL-4-induced macrophage M2 polarization and fibrosis.
Int J Biol Sci
January 2025
Department of Respiratory and Critical Care Medicine, National Clinical Research Center of Respiratory Disease, Key Laboratory of Pulmonary Diseases of Health Ministry, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
As a leading cause of morbidity and mortality, fibrosis is the common pathway of various chronic inflammatory diseases in organs and causes death in a large number of patients. It can destroy the structure and function of organs and ultimately lead to organ failure, which is a major cause of disability and death in many diseases. However, the regulatory mechanism of organ fibrosis is not well clear and the lack of effective drugs and treatments, which seriously endangers human health and safety.
View Article and Find Full Text PDFInsulin-Like Growth Factor-1 (IGF-1) Deficiency and Metabolic-Dysfunction-Associated Steatotic Liver Disease in a Young Patient.
Cureus
January 2025
Genetics Clinic, Karaiskakio Foundation, Nicosia, CYP.
Metabolic-dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease in the Western world. MASLD-associated cirrhosis prevalence is on the rise along with the obesity and metabolic syndrome epidemic. Genetic factors are included in the multi-hit model of MASLD pathogenesis and insulin-like growth factor-1 (IGF-1) has an important role.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!