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Microenvironment-induced programmable nanotherapeutics restore mitochondrial dysfunction for the amelioration of non-alcoholic fatty liver disease.
Acta Biomater
January 2025
Key Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China; Shandong Key Laboratory of Endocrinology and Lipid Metabolism, Jinan, Shandong, 250021, China; Shandong Engineering Laboratory of Prevention and Control for Endocrine and Metabolic Diseases, Jinan, Shandong, 250021, China. Electronic address:
Nonalcoholic fatty liver disease (NAFLD) is a metabolic liver disorder with severe complications. Mitochondrial dysfunction due to over-opening of the mitochondrial permeability transition pore (mPTP) in liver cells plays a central role in the development and progression of NAFLD. Restoring mitochondrial function is a promising strategy for NAFLD therapy.
View Article and Find Full Text PDFRole of AIM2 and cGAS-STING signaling in high fat high carbohydrate diet-induced gut dysbiosis associated neurodegeneration.
Life Sci
January 2025
Department of Pharmacology & Toxicology, National Institute of Pharmaceutical Education and Research, Chunilal Bhawan, 168, Maniktala Main Rd, Kolkata, West Bengal 700054, India. Electronic address:
Aims: Gut dysbiosis modulates CNS complications and cognitive decline through the gut-brain axis. The study aims to investigate the molecular mechanisms involved in gut dysbiosis-associated cognitive changes and the potential effects of probiotics in high fat-high carbohydrate diet-induced gut dysbiosis-associated neurodegeneration.
Materials And Methods: We used high fat, high-carbohydrate diet (HFHCD) and high-fat diet (HFD) to induce gut dysbiosis-associated neurodegeneration in C57BL/6 mice.
Traditional Chinese Medicine Borneol-Based Polymeric Micelles Intracerebral Drug Delivery System for Precisely Pathogenesis-Adaptive Treatment of Ischemic Stroke.
Adv Sci (Weinh)
January 2025
Frontiers Science Center for Deep Ocean Multispheres and Earth Systems, Key Laboratory of Marine Chemistry Theory and Technology, Ministry of Education/Sanya Oceanographic Institution, Ocean University of China, Qingdao/Sanya, 266003/572024, China.
The scarcity of effective neuroprotective agents and the presence of blood-brain barrier (BBB)-mediated extremely inefficient intracerebral drug delivery are predominant obstacles to the treatment of cerebral ischemic stroke (CIS). Herein, ROS-responsive borneol-based amphiphilic polymeric NPs are constructed by using traditional Chinese medicine borneol as functional blocks that served as surface brain-targeting ligand, inner hydrophobic core for efficient drug loading of membrane-permeable calcium chelator BAPTA-AM, and neuroprotective structural component. In MCAO mice, the nanoformulation (polymer: 3.
View Article and Find Full Text PDFBisphenol A induces apoptosis and disrupts testosterone synthesis in TM3 cells via reactive oxygen species-mediated mitochondrial pathway and autophagic flux inhibition.
Ecotoxicol Environ Saf
January 2025
College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Harbin 150030, China. Electronic address:
Bisphenol A (BPA) is a common endocrine disruptor chemical that is widely used in the production of food plastic packaging, and it has been shown to potentially harm the reproductive system. However, the specific mechanism by which BPA induces apoptosis of Leydig cells (LCs) and inhibits testosterone synthesis in these cells is unclear. In the present study, TM3 cells were used as an experimental model in combination with a reactive oxygen species (ROS) scavenger (N-acetylcysteine), Caspase-3 inhibitor (Ac-DEVD-CHO), autophagy activator (Torin2), and autophagy inhibitor (Chloroquine) to investigate the potential mechanisms by which BPA causes TM3 cell damage in vitro.
View Article and Find Full Text PDFDisease stage-specific role of the mitochondrial pyruvate carrier suppresses differentiation in temozolomide and radiation-treated glioblastoma.
Neuro Oncol
January 2025
Department of Pathology, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada.
Article Synopsis
- The mitochondrial pyruvate carrier (MPC) plays a key role in connecting glycolysis to mitochondrial metabolism and its function in glioblastoma (GBM) post-treatment is not well understood.
- Through in vitro and in vivo studies, the research shows that the MPC is crucial in regulating metabolism after treatments like temozolomide (TMZ) and radiation, specifically inhibiting differentiation in GBM cells.
- The study highlights the potential for using MPC inhibitors to enhance the effectiveness of current therapies and improve survival rates for GBM patients.
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