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Background/aim: Curcumin is a polyphenol that exerts a variety of pharmacological activities and plays an anti-cancer role in many cancer cells. It was recently reported that gasdermin E (GSDME) is involved in the progression of pyroptosis.
Materials And Methods: HepG2 cells were treated with various concentrations of curcumin and cell viability was examined using MTT assay, apoptosis was analysed using flow cytometry, reactive oxygen species (ROS) levels using dihydroethidium, LDH release using an LDH cytotoxicity assay, and protein expression using western blot.
Results: Curcumin increased the expression of the GSDME N-terminus and proteins involved in pyrolysis, promoted HspG2 cell pyrolysis and increased intracellular ROS levels. Moreover, inhibition of the production of intracellular ROS with n-acetylcysteine (NAC) improved the degree of apoptosis and pyrolysis induced by curcumin.
Conclusion: Curcumin induces HspG2 cell death by increasing apoptosis and pyroptosis, and ROS play a key role in this process. This study improves our understanding of the potential anti-cancer properties of curcumin in liver cancer.
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http://dx.doi.org/10.21873/invivo.12253 | DOI Listing |
Front Pharmacol
August 2025
Department of Medicament, College of Medicine, Xizang University, Lhasa, China.
Background: (Benth.) Baker is a perennial shrub endemic to the Tibetan Plateau. Its seeds are traditional Tibetan medicine for treating jaundice, hepatitis, purulent tonsillitis, diphtheria, and parasitosis.
View Article and Find Full Text PDFDalton Trans
September 2025
Biomedical Inorganic Chemistry Lab, Department of Chemical Sciences, University of Catania, v.le A. Doria 6, 95125, Catania, Italy.
Current anticancer therapy is challenged by the adaptability and resistance of tumor cells as well as limited drug selectivity that causes severe side effects. The scientific community maintains high interest in metal-based chemotherapeutic agents due to their unique interactions with cancer cells, potentially overcoming resistance mechanisms and exploiting the physiopathology of the tumour tissues. Copper, in particular, plays a dual role in cancer, both facilitating tumor progression and triggering cuproptosis, a copper-induced cell death mechanism.
View Article and Find Full Text PDFEur J Med Chem
August 2025
School of Chemistry and Chemical Engineering, Anhui University of Technology, Ma'anshan, 243032, Anhui, PR China. Electronic address:
Cancer remains a leading global cause of mortality, with treatment efficacy often compromised by drug resistance, highlighting the urgent need for novel targeted therapies. The enzyme fructose-2,6-bisphosphatase 4 (PFKFB4) governs glycolytic flux by modulating fructose-2,6-bisphosphate (F2,6BP) levels. PFKFB4 overexpression has been observed in various cancers and correlates with tumor growth, aggressiveness, and poor prognosis.
View Article and Find Full Text PDFXenobiotica
September 2025
Department of Pharmacy, Binhai County People's Hospital, Yancheng 224500, China.
To study the effects of calycosin on palmitic acid-induced HepG2 cells, as well as the potential mechanisms of action. Potential targets of calycosin for the alleviation of insulin resistance were predicted by network pharmacology. Glucose concentration in the culture medium was determined by the GOD-POD method.
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September 2025
Faculty of Chemistry, Nicolaus Copernicus University in Toruń, Gagarina 7, 87-100 Toruń, Poland.
This study comprehensively analyses two new ruthenium(III) complexes, [RuCl(Nic)][(CH)NH]DMF, 1, and [RuCl(3-HPA)][3-HHPA](EtOH), 2, (where Nic = nicotinic acid (vitamin B3), 3-HPA = anion of a 3-hydroxypicolinic acid), as potential antimicrobial agents, highlighting their physicochemical properties, nanoparticle formation, and cytotoxic activity. The complexes were fully characterised by a single crystal X-ray diffraction technique, Fourier-transform infrared, energy-dispersive X-ray, and electron paramagnetic resonance spectroscopies. The synthesis of micro- and nanoparticles (NPs) of these complexes was performed using the liquid anti-solvent crystallisation method.
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