Objective: To study the expression of hepatic Bcl-2 and Bax proteins in mice infected with Schistosoma japonicum and the role of pentoxifylline (PTX) in the expression.
Methods: Forty mice were randomly divided into 4 groups: one normal control group,mice in the other three groups were all infected each with 25 cercariae, the infected control group was fed for 10 weeks after infection, and 2 weeks after infection, the high dose PTX group was given PTX 360 mg/(kg x d) for 8 weeks and the low dose PTX group was given PTX 180 mg/(kg x d)also for 8 weeks. At the end of 10 weeks all the mice were killed. Bcl-2 and Bax proteins expression was detected by immunohistochemisty.
Results: Compared with the normal control group, the expression of Bcl-2 and Bax was significantly higher in the infected control group (P < 0.05). Bcl-2 was significantly higher in high (dose PTX group than in the infected control group and in low dose PTX group (P < 0.05). However there was no significant difference in the expression of Bax among the groups (P > 0.05).
Conclusion: PTX treatment can significantly increase the expression of Bcl-2 in liver tissue of schistosome-infected mice in a dose-dependent manner, and may play a role against liver inflammation and schistosomiasis-related liver fibrosis.
Download full-text PDF |
Source |
---|
Cytotechnology
February 2025
Department of Neurology, Hubei Provincial Hospital of Integrated Traditional and Western Medicine, Jianghan District, No. 11 Lingjiaohu Road, Wuhan, 430015 China.
Unlabelled: Alzheimer's disease (AD) is a progressive neurological condition that causes brain shrinkage and cell death. This study aimed to identify the role of the NORAD/miR-26b-5p axis in AD. StarBase was used to examine the binding sequences of miR-26b-5p to LncRNA NORAD or its target genes, which were verified by a double luciferase reporter assay.
View Article and Find Full Text PDFFood Sci Nutr
January 2025
Agricultural Extension Directorate, MAAR Damascus Syria.
Coumarins, a group of naturally occurring compounds, have been reported to demonstrate anticancer potential. These substances, distinguished by their combined benzene and α-pyrone rings, have been demonstrated to impact multiple cellular mechanisms essential for the initiation and advancement of cancer. These agents work in different ways that prevent different tumor cells from growing, spreading, and increasing.
View Article and Find Full Text PDFQuinoa saponins can inhibit the survival of specific cancer cells. However, there is still a lack of systematic research on the effects of quinoa saponins on colon cancer cells. This experiment confirmed that quinoa saponins prevented human colon cancer HT-29 cells from growing in vitro.
View Article and Find Full Text PDFToxicol Rep
June 2025
Pharmcology Department, Theodor Bilharz Research Institute, Giza, Egypt.
Ulcerative colitis (UC), a persistent immune-mediated disorder lacking effective treatment, is distinguished by gut microbiota dysbiosis, abnormal activation of the NLRP3 inflammasome pathway, and apoptosis. Despite growing attention to these factors, understanding their significance in UC pathogenesis remains a challenge. The present study explores the potential therapeutic impact of (Bc) spores in a murine UC model induced by drinking 4 % (w/v) dextran sulfate sodium (DSS) in C57BL/6 mice.
View Article and Find Full Text PDFJ Inflamm Res
January 2025
Department of Orthopaedics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, People's Republic of China.
Background: Osteoarthritis (OA) is a leading cause of pain, disability, and reduced mobility worldwide, characterized by metabolic imbalances in chondrocytes, extracellular matrix (ECM), and subchondral bone. Emerging evidence highlights the critical role of long non-coding RNAs (lncRNAs) in OA pathogenesis. This study focuses on lncRNA PTS-1, a novel lncRNA, to explore its function and regulatory mechanisms in OA progression.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!