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Kirenol alleviates cerebral ischemia-reperfusion injury by reducing oxidative stress and ameliorating mitochondrial dysfunction via activating the CK2/AKT pathway.
Free Radic Biol Med
March 2025
Institute of Structural Pharmacology & TCM Chemical Biology, Fujian Key Laboratory of Chinese Materia Medica, College of Pharmacy, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China; Wuya College of Innovation, School of Pharmacy, Key Laboratory of Structure-Based Drug Design & Discovery, Ministry of Education, Shenyang Pharmaceutical University, Shenyang, Liaoning 110016, China. Electronic address:
Ischemic stroke represents a predominant cause of morbidity and mortality globally, resulting from abrupt vascular occlusion or rupture, which precipitates considerable neuronal damage. This study aims to shed more light on the specific neuroprotective mechanisms of Kirenol, a bioactive diterpene derived from traditional herbal medicine, with a particular focus on its regulation of mitochondrial dynamics via the CK2/AKT signalling pathway and its impact on the mitochondrial fusion protein Optic atrophy 1 (Opa1). The effects of Kirenol on neuronal viability, mitochondrial function, and pertinent signalling pathways were evaluated by employing a middle cerebral artery occlusion (MCAO) model in rats and subjecting HT22 neuronal cells to oxidative stress.
View Article and Find Full Text PDFChemotoxic and phototoxic effects of liposomal co-delivery of green synthesized silver nanoparticles and ZnPcS for enhanced photodynamic therapy in MCF-7 breast cancer cells: An in vitro study.
Biomed Pharmacother
March 2025
Laser Research Centre, Faculty of Health Sciences, University of Johannesburg, P.O. Box 17011, Doornfontein 2028, South Africa. Electronic address:
Breast cancer remains a significant challenge in oncology, despite notable advances in treatment methods. Traditional therapies such as surgery, chemotherapy, radiation, and hormonal treatments have long been used to manage breast cancer. However, often patients experience treatment failure, resulting in disease recurrence and progression.
View Article and Find Full Text PDFSynthesis and biological evaluation of the Fluoro analog of Romidepsin with improved selectivity for class I histone deacetylases (HDACs).
Bioorg Chem
March 2025
School of Pharmacy, Fudan University; 826 Zhangheng Road, Pudong Zone, Shanghai 201203, China.
Selective inhibition of Class I HDACs has emerged as a promising approach for cancer therapy. Building on our previous work with Largazole (a member of the natural depsipeptide family), we have applied a similar fluorination modification to Romidepsin and synthesized its fluoro analog (12) in 12 steps. This analog exhibits potent inhibitory activity against Class I HDACs but shows no inhibitory effect on HDAC6, confirming its selectivity as a Class I HDAC inhibitor (IC50 HDAC1 0.
View Article and Find Full Text PDFFangchinoline suppresses nasopharyngeal carcinoma progression by inhibiting SQLE to regulate the PI3K/AKT pathway dysregulation.
Phytomedicine
February 2025
Dongguan Hospital of Traditional Chinese Medicine (Department of Internal Medicine IX), No. 3 Songshan Lake Avenue East Section, Dongcheng Street, Dongguan City, Guangdong Province, China. Electronic address:
Background And Purpose: Squalene epoxidase (SQLE), a key enzyme in cholesterol metabolism, remains underexplored in nasopharyngeal carcinoma (NPC). Additionally, the therapeutic potential of Fangchinoline, an alkaloid with anticancer properties, has yet to be systematically evaluated. This research investigates Fangchinoline's efficacy in NPC treatment and SQLE-related mechanisms.
View Article and Find Full Text PDFPeritubular Myoid Cells of the Testis Produce Monocyte Chemotactic Protein 1 Upon Direct Exposure to Mono-(2-Ethylhexyl) Phthalate Through the IL-1 Signaling Pathway.
Toxicology
March 2025
Division of Pharmacology and Toxicology, College of Pharmacy, University of Texas at Austin, Austin, TX, 78712, USA.
Mono-(2-ethylhexyl) phthalate (MEHP) is a metabolite of the diester parent compound Di(2-ethylhexyl) phthalate (DEHP), a widespread environmental toxicant known for its harmful effects on Sertoli cells and the subsequent loss of germ cells through apoptosis in postnatal animals. Peritubular myoid cells (PTMCs) produce various signaling factors, including the chemokine monocyte chemotactic protein 1 (MCP-1); however, the MEHP exposure-induced BTB disruption followed by MCP-1 secretion by PTMCs, the recruitment, and activation of macrophages as well as molecular mechanisms that initiate the secretion in the testis has yet to be closely examined. In this study, we demonstrate for the first time that PTMCs generate MCP-1 via the interleukin-1 signaling pathway upon MEHP exposure.
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