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Cancers, Vol. 13, Pages 1216: Cache Domain Containing 1 Is a Novel Marker of Non-Alcoholic Steatohepatitis-Associated Hepatocarcinogenesis
Hideki Wanibuchi In the present study, potential molecular biomarkers of NASH hepatocarcinogenesis were investigated using the STAM mice NASH model, characterized by impaired insulin secretion and development of insulin resistance. In this model, 2-days-old C57BL/6N mice were subjected to a single subcutaneous (s.c.) injection of 200 μg streptozotocin (STZ) to induce diabetes mellitus (DM). Four weeks later, mice were administered high-fat diet (HFD) HFD-60 for 14 weeks (STAM group), or fed control diet (STZ group). Eighteen-week-old mice were euthanized to allow macroscopic, microscopic, histopathological, immun...
Source: Cancers - March 10, 2021 Category: Cancer & Oncology Authors: Anna Kakehashi Arpamas Chariyakornkul Shugo Suzuki Napaporn Khuanphram Kumiko Tatsumi Shotaro Yamano Masaki Fujioka Min Gi Rawiwan Wongpoomchai Hideki Wanibuchi Tags: Article Source Type: research

Activation of the AMPK-SIRT1 pathway contributes to protective effects of Salvianolic acid A against lipotoxicity in hepatocytes and NAFLD in mice
Conclusion: Our data uncover a novel mechanism for hepatoprotective effects of Sal A against lipotoxicity both in livers from HFCD-fed mice and palmitic acid-treated hepatocytes.
Source: Frontiers in Pharmacology - November 30, 2020 Category: Drugs & Pharmacology Source Type: research

Tangshen Formula Alleviates Hepatic Steatosis by Inducing Autophagy Through the AMPK/SIRT1 Pathway
Conclusion In conclusion, the present study demonstrated that autophagy was involved in relieving the effects of TSF against NAFLD, which were mediated by the AMPK/SIRT1 pathway (Figure 7D). These findings may improve our current understanding of the role of TSF in treating hepatic steatosis and provide an experimental basis for the clinical application of TSF in NAFLD and its related metabolic syndrome. Ethics Statement This study was carried out in accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health. The protocol was approved by the Ethics Co...
Source: Frontiers in Physiology - April 25, 2019 Category: Physiology Source Type: research

TonEBP Suppresses the HO-1 Gene by Blocking Recruitment of Nrf2 to Its Promoter
Discussion Dynamic changes in the functional phenotype of macrophages are associated with pathogenesis of inflammatory diseases (5–7). TonEBP primes macrophages toward an M1 phenotype, which has pro-inflammatory properties. TonEBP does this by promoting expression of pro-inflammatory genes via interaction with NF-κB (36) and by binding directly to the promoter (37, 64). In addition, TonEBP suppresses expression of the anti-inflammatory cytokine IL-10 by limiting chromatin access to the promoter (37). The pro-inflammatory function of TonEBP suggests that inhibiting its expression or activation could suppres...
Source: Frontiers in Immunology - April 17, 2019 Category: Allergy & Immunology Source Type: research

Repin1 deficiency in liver tissue alleviates NAFLD progression in mice
This study provides evidence that loss of Repin1 in the liver attenuates NAFLD progression, most likely by reducing fat accumulation and alleviating chronic tissue inflammation. Thus, modulating Repin1 expression may become a novel strategy and potential tool to inhibit NAFLD progression.Graphical abstract
Source: Journal of Advanced Research - November 23, 2018 Category: Research Source Type: research

Clofibrate Attenuates ROS Production by Lipid Overload in Cultured Rat Hepatoma Cells.
CONCLUSIONS: Characteristic cellular damage resulted from released ROS following a high fat load to hepatoma cells. The damage was attenuated through early treatment with clofibrate, which may act as a hepatoprotectant by inducing FABP1 expression and in this manner, suppress intracellular ROS levels. This article is open to POST-PUBLICATION REVIEW. Registered readers (see "For Readers") may comment by clicking on ABSTRACT on the issue's contents page. PMID: 28810950 [PubMed - in process]
Source: Journal of Pharmacy and Pharmaceutical Sciences - August 18, 2017 Category: Drugs & Pharmacology Tags: J Pharm Pharm Sci Source Type: research