Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/0006-291x(70)90654-6 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Vitamin D3/VDR alleviates double-stranded RNA virus -induced biliary epithelial cell damage by inhibiting autophagy.
BMC Gastroenterol
January 2025
Department of Pediatrics, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, 710061, China.
Background: The increased apoptosis of bile duct epithelial cells (BECs) due to some damage factors is considered the initiating factor in the occurrence and progression of biliary atresia (BA). Vitamin D receptor (VDR) is thought to play a crucial role in maintaining the intrinsic immune balance and integrity of bile duct epithelial cells (BECs). To investigate the role of VDRs in the pathogenesis and progression of BA using in vitro and in vivo models.
View Article and Find Full Text PDFThe PPAR-α agonist oleoyethanolamide (OEA) ameliorates valproic acid-induced steatohepatitis in rats via suppressing Wnt3a/β-catenin and activating PGC-1α: Involvement of network pharmacology and molecular docking.
Eur J Pharmacol
January 2025
Pharmacology & Environmental Toxicology, Environmental Studies & Research Institute (ESRI), University of Sadat City, Sadat City 32897, Menoufia, Egypt. Electronic address:
Liver damage is one of the most severe side effects of valproic acid (VPA) therapy. Research indicates that PPAR-α prevents Wnt3a/β-catenin-induced PGC-1α dysregulation, which is linked to liver injury. Although PPAR-α activation has hepatoprotective effects, its role in preventing VPA-induced liver injury remains unclear.
View Article and Find Full Text PDFShort-term starvation boosts anti-PD-L1 therapy by reshaping tumor-associated macrophages in hepatocellular carcinoma.
Hepatology
January 2025
Hepatic Surgery Centre, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, People's Republic of China.
Background And Aims: Immune checkpoint inhibitors (ICIs) have revolutionized systemic hepatocellular carcinoma (HCC) treatment. Nevertheless, numerous patients are refractory to ICIs therapy. It is currently unknown whether diet therapies such as short-term starvation (STS) combined with ICIs can be used to treat HCC.
View Article and Find Full Text PDFCD155 promotes the advancement of hepatocellular carcinoma by suppressing the p53-mediated ferroptosis via interacting with CD96.
J Mol Med (Berl)
January 2025
Hospital Sensory Department, Shenzhen Qianhai Shekou Free Trade Zone Hospital, 36 Gongye Qi Road, Nanshan District, Shenzhen, 518067, China.
This work researched the influence and mechanism of CD155 on hepatocellular carcinoma advancement. CD155 expression and its effect on survival of hepatocellular carcinoma patients were analyzed based on the GEPIA2 database. String software predicted the interacting between CD155 and CD96, which was further verified by co-immunoprecipitation experiment.
View Article and Find Full Text PDFWhole blood exchange ameliorates acute hemolytic anemia by reducing inflammation and oxidative stress in rats.
FASEB J
January 2025
Department of Blood Transfusion, Xiangya Hospital, Central South University, Changsha, China.
Hemolytic anemia (HA) is characterized by massive destruction of red blood cells (RBCs) and insufficient oxygen supply, which can lead to shock, organ failure, even death. Recent studies have preliminarily demonstrated the therapeutic effectiveness of whole blood exchange (WBE) in the management of acute hemolytic anemia and exhibited potential for reducing the duration of corticosteroid treatment, while the underlying mechanism of WBE therapy was not investigated in preclinical study. Hence, we investigate the therapeutic mechanisms of WBE in HA through established continued WBE therapy in rats creatively.
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!