Objective: To study the anti-proliferation effect of Taraxacum mongolicum extract in HepG2 cells and its mechanism.
Methods: The total proteins of HepG2 cells treated with Taraxacum mongolicum extract were. extracted and mitochondria-mediated apoptosis-related proteins (Survivin, Mcl-1, BCL-xL, BCL-2, Smac, BAX, Bad, Cytochrome c and Caspase-3/7/9) were detected by Western blot.
Results: Taraxacum mongolicum extract obviously inhibited the proliferation of HepG2 cells and the expression of anti-apoptotic proteins (Survivin, BCL-xL and BCL-2), increased the expression of pro-apoptotic proteins (Smac and Caspase-3/7/9), and promoted the release of Cytochrome c from mitochondria to cytoplasm in HepG2 cells. The effects were in a dose-independent mode.
Conclusion: Taraxacum mongolicum extract can inhibit the proliferation of HepG2 cells and the anti-proliferation mechanism is related to mitochondria-mediated apoptosis.
Download full-text PDF |
Source |
---|
Chem Biodivers
January 2025
Guangxi Science and Technology Normal University, School of food biochemical engineering, Tiebei road 966, 546199, Laibin, CHINA.
Although cisplatin is widely used as a first-line chemotherapy agent, it has significant side effects. Herein, we synthesized a Pt(II) complex (Pt1) derived from o-vanillin-4-phenylthiosemicarbazone ligand, and confirmed its crystal structure by X-ray crystallography. Complex Pt1 exhibited potent anticancer activity against various tested cancer cell lines, with particular efficacy against HepG-2 cells.
View Article and Find Full Text PDFMol Omics
January 2025
Department of Biotechnology, Thapar Institute of Engineering and Technology, Patiala, Punjab, India.
The present work aimed to examine the primary mechanisms of liver damage, namely the impact of gut-derived endotoxins along the gut-liver axis and adipose-derived free fatty acids along the adipose-liver axis. These processes are known to play a significant role in the development of hepatic inflammation and steatosis. Although possible overlapping in the pathogenesis was expected, these processes have unique pathophysiological consequences.
View Article and Find Full Text PDFFree Radic Biol Med
December 2024
Institute of Biomedicine of Seville (IBiS), Hospital University "Virgen del Rocío"/CSIC/University of Seville, Seville, Spain; Department of Medical Physiology and Biophysics, University of Seville, Seville, Spain; Biomedical Research Center for Hepatic and Digestive Diseases (CIBERehd), Madrid, Spain. Electronic address:
Background: Sorafenib is a tyrosine kinase inhibitor (TKI) that belongs to the landscape of treatments for advanced stages of hepatocellular carcinoma (HCC). The induction of cell death and cell cycle arrest by Sorafenib has been associated with mitochondrial dysfunction in liver cancer cells. Our research aim was to decipher underlying oxidative and nitrosative stress induced by Sorafenib leading to mitochondrial dysfunction in liver cancer cells.
View Article and Find Full Text PDFBiochim Biophys Acta Mol Basis Dis
December 2024
Department of Emergency Medicine, Second Affiliated Hospital, Department of Epidemiology and Biostatistics, School of Public Health, The Key Laboratory of Intelligent Preventive Medicine of Zhejiang Province, Zhejiang University School of Medicine, Hangzhou, China. Electronic address:
Background & Aims: Given the impact of nonalcoholic fatty liver disease (NAFLD) on T cell activation and proliferation functions, we aim to explore the heterogeneity of follicular cytotoxic T (Tfc) cells in chronic hepatitis B (CHB) patients with NAFLD.
Methods: 32 healthy controls (HCs), 36 treatment-naïve CHB patients, and 19 treatment-naïve CHB + NAFLD patients were recruited. We employed multicolor flow cytometry to assess the exhausted phenotype and functionality of Tfc cells.
Food Chem
December 2024
Anhui Province Key Laboratory of Environmental Toxicology and Pollution Control Technology; High Magnetic Field Laboratory, HFIPS, Chinese Academy of Science, Hefei, Anhui 230031, PR China. Electronic address:
Micro- and nanoplastics (MNPs) released from plastic containers pose significant food safety concerns; however, their release patterns in different containers along with their impacts on other pollutants remain poorly understood. This study revealed that feeding bottles, food containers, and paper cups released approximately 10 microplastics and 10 nanoplastics after hot water treatment. These released MNPs were nontoxic in six cell types, whereas they significantly amplified the toxicity of disinfection by-products (DBPs), a widely existing contaminant in drinking water.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!