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Purpose: Effectively controlling the accumulation of adipose tissue can be a therapeutic strategy for treating obesity, which is a global problem. The present study was designed for comparative assessment of antiobesity activities of the -dichloromethane seed extract (DCME) and the isolated phytochemicals, bakuchiol, isopsoralen, and psoralen, through antiadipogenesis and pancreatic lipase (PL) inhibition assays. pancreatic lipase activity was determined spectrophotometrically by measuring the hydrolysis of -nitrophenyl butyrate (-NPB) to -nitrophenol at 405 nm, and adipogenesis was assayed in 3 T3-L1 adipocytes (by using Oil Red O staining) using -dichloromethane seed extract (DCME) and individual compounds, isolated from the extract.
Result: Antilipase as well as antiadipogenesis activity was displayed by both the DCME and the compounds. Maximum antilipase property was recorded in DCME (26.02 ± .041%) at 100 g/ml, while, among the isolated compounds, bakuchiol exhibited a higher activity (24.2 ± 0.037%) at 100 g/ml concentration, compared to other isolates. DCME was found to exhibit antiadipogenesis property, 75 ± 0.003% lipid accumulation, compared to the control at 100 g/ml dose. Bakuchiol, isopsoralen, and psoralen inhibited the lipid accumulation in 3T3-L1 preadipocytes, 78.06 ± 0.002%, 80.91 ± 0.004%, and 80.91 ± 0.001%, respectively, lipid accumulation in comparison to control at 25 M dose.
Conclusion: The present study highlights the antiobesity potential of and its active constituents. Thus, it can be concluded that has the potential to treat obesity and related diseases; however, further research on dose standardization and clinical trials are required.
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http://dx.doi.org/10.1155/2022/9504787 | DOI Listing |
Arterioscler Thromb Vasc Biol
September 2025
Vascular Biology Program, Boston Children's Hospital and Harvard Medical School, MA (K. Cui, B.Z., B.W., S.E.-B., A.V., H.C.).
Background: Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipid-laden foam cells and plaques within the arterial wall. Dysfunctional vascular smooth muscle cells (VSMCs), fibroblasts, endothelial cells, and macrophages contribute to disease progression. Here, we report that macrophage-specific expression of epsins, highly conserved endocytic adaptor proteins involved in clathrin-mediated endocytosis, accelerates atherosclerosis in Western diet-fed mice.
View Article and Find Full Text PDFTrends Biochem Sci
September 2025
Department of Biochemistry and Molecular Biology, University of Nevada, Reno, NV, USA. Electronic address:
Huntington's disease (HD) is a neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin (HTT) gene, resulting in an expanded polyglutamine (polyQ) tract in HTT protein. Expanded polyQ tracts cause mutant HTT (mHTT) to aggregate and accumulate as cellular inclusions. Recent studies highlight the interactions between mHTT and different cellular membranes that contribute to HD pathogenesis.
View Article and Find Full Text PDFAdv Med Sci
September 2025
Clinical Department of Diabetology, Hypertension and Internal Diseases, Institute of Internal Diseases, Wroclaw Medical University, Wroclaw, Poland.
Atherosclerosis is a progressive process resulting from endothelial dysfunction, primarily caused by damage to the integrity of the glycocalyx. Its pathogenesis is complex and involves numerous biomechanical and biochemical factors, such as blood pressure, shear forces, lipid metabolism disorders, monocyte migration and their transformation into macrophages, immune response, lipid accumulation, neovascularization, and activation of coagulation. Recently, the possibility of atherosclerosis regression has been confirmed, although the mechanisms behind the reversal of changes remain unknown.
View Article and Find Full Text PDFJ Adv Res
September 2025
School of Public Health and Nursing, Zhejiang Key Laboratory of Medical Epigenetics, Hangzhou Normal University, Hangzhou, China. Electronic address:
Introduction: Metabolic dysfunction-associated steatotic liver disease (MASLD) represents an increasing global health problem in association with obesity and insulin resistance without approved pharmacotherapy. Previous studies revealed malic enzyme 1 (ME1) as a susceptibility gene for metabolic disorders in humans. However, the role and mechanisms of ME1 in regulating hepatic lipid metabolism remain largely unclear.
View Article and Find Full Text PDFFitoterapia
September 2025
Yunnan Key Laboratory of Southern Medicine Utilization, College of Traditional Chinese Medicine, Yunnan University of Chinese Medicine, Kunming 650500, China. Electronic address:
The gut microbiota and its products are recognized as pivotal contributors to the pathogenesis of metabolic-associated fatty liver disease (MAFLD). Shenling Jianpiwei formula (SLJPW), a prescription renowned for its protective effects in intestinal disorders, demonstrates efficacy against MAFLD. However, its underlying mechanisms and chemical composition remain unclear.
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