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Non-alcoholic fatty liver disease (NAFLD) involves lipid accumulation in liver without consumption of alcohol and affects many people worldwide. NAFLD is associated with metabolic syndrome disease such as obesity, insulin resistance, hyperlipidemia, and diabetes. However, there are no pharmacologic therapies for NAFLD. Recently, there are increasing reports that several natural plants can inhibit lipid accumulation in hepatocytes. Bay laurel ( L.) leaves have been used in traditional medicine for rheumatism, stomach ache, emetic, skin rashes, and earaches. Our objective was to investigate the effect of bay laurel leaves water extract (BLW) on free fatty acid (FFA) treated hepatocyte and high fructose, high fat (HFHF) diet in a mouse model of NAFLD. , lipid accumulation increased only in the FFA treated group, while BLW reduced lipid accumulation to a level comparable to that only in the FFA treated group. Cellular antioxidants were increased in the BLW compared to the only FFA-treated group, but cellular MDA levels were decreased in the BLW compared to the only FFA treated group. Cellular lipid accumulation, inflammation, and apoptosis were reduced in the BLW compared to the only FFA treated group. , serum ALT, AST, and GGT levels in the BLW supplementation group were significantly decreased compared with the HFHF group. Hepatic TC, TG, and MDA levels were significantly decreased in the HFHF+100 and HFHF+200 groups compared to the HFHF group. The hepatic antioxidant activities in the BLW supplementation groups were significantly increased compared to the HFHF group. The expression of proteins related to hepatic inflammation and apoptosis was reduced in the BLW supplementation groups compared to the HFHF group. These results suggest that BLW could be potentially useful in the treatment of NAFLD due to its inhibitory effects on hepatic lipogenesis, hepatic inflammation, and hepatic apoptosis.
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http://dx.doi.org/10.29219/fnr.v69.10668 | DOI Listing |
Toxicol Appl Pharmacol
September 2025
Department of Environmental Hygiene and Toxicology, School of Public Health, Wenzhou Medical University, Wenzhou 325035, China. Electronic address:
Phthalates (PEs) are widespread in environment, and human beings are unavoidably exposing to the mixture of PEs, which may induce male reproductive health risks. In order to investigate the mechanism of male reproductive injuries caused by the mixture of di-2-ethylhexyl phthalate, dibutyl phthalate and butyl benzyl phthalate (MPEs), male rats were orally exposed to 16 mg/kg/d MPEs (L-MPEs) and 450 mg/kg/d MPEs (H-MPEs) for 90 days, and the results showed that MPEs decreased the weights of testes, epididymis and periepididymis fat, decreased serum levels of male hormones, increased abnormal sperm rate, and caused testicular histopathological damages, such as atrophy and cavitation of seminiferous tubules, spermatids exfoliation, Leydig cells hyperplasia and accumulation of lipid droplets in the testicular interstitium. Testicular transcriptomic analysis identified 100 differently expressed genes (DEGs) in L-MPEs group and 10,880 DEGs in H-MPEs group, and these DEGs mainly involved in signaling pathways of focal adhesion, PI3K-Akt, AGE-RAGE, axon guidance, PPAR, MAPK and etc.
View Article and Find Full Text PDFArch Biochem Biophys
September 2025
Department of Hematology, Shidong Hospital, Yangpu District, Shidong Hospital Affiliated to University of Shanghai for Science and Technology, Shanghai, China 200433. Electronic address:
Background: Benzene, a ubiquitous industrial chemical, is a well-established environmental toxin associated with hematological disorders such as myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML), which are characterized by impaired hematopoiesis and bone marrow failure. This study investigates the role of ferroptosis, an iron-dependent form of cell death, in benzene-induced hematotoxicity, focusing on the repression of glutathione peroxidase 4 (GPX4), a critical regulator of ferroptosis.
Materials And Methods: Male C57BL/6 mice were exposed to benzene at various doses over six weeks.
J Adv Res
September 2025
State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi International Joint Research Center for Oral Diseases, Department of Oral Anatomy and Physiology and TMD, School of Stomatology, The Fourth Military Medical Univ
Introduction: Aberrant biomechanical force-induced chondrocyte adipogenesis is involved in the development of temporomandibular joint osteoarthritis (TMJ OA). Growth differentiation factor 11 (GDF11) has been implicated in this process. However, whether mechanosensitive histone deacetylase 3 (HDAC3) regulates GDF11 signaling in the context of TMJ OA remains to be elucidated.
View Article and Find Full Text PDFJ Adv Res
September 2025
National Medical Products Administration (NMPA) Key Laboratory for Safety Evaluation of Cosmetics, Guangdong Provincial Key Laboratory of Tropical Disease Research, Department of Toxicology, School of Public Health, Southern Medical University, Guangzhou, China. Electronic address: huangzhenlie85825
Introduction: The increasing use of biodegradable plastics has led to the inevitable human consumption of biodegradable microplastics (MPs). These MPs can be degraded and absorbed into various organs and tissues via the gastrointestinal tract, with the liver being the primary target for digestion and absorption.
Objectives: This study aimed to investigate the toxic effects and mechanisms of biodegradable MPs on the liver following gastrointestinal degradation.
Environ Int
September 2025
Division of Gastrointestinal and Liver Diseases, Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States. Electronic address:
Background: Although per- and polyfluoroalkyl substances (PFAS) have been linked to chronic liver diseases, the specific cellular and molecular mechanisms by which different PFAS contribute to human liver dysfunction remain unclear. This study aims to elucidate those mechanisms.
Methods: We exposed a multi-donor human liver spheroid model composed of multiple cell types to 20 µM of PFHxS, PFOA, PFOS, or PFNA for seven days, followed by single-cell RNA sequencing and lipid staining.