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      Inhibition of HepG2 cell proliferation by ursolic acid and polysaccharides via the downregulation of cyclooxygenase-2.

      Molecular Medicine Reports
      Apoptosis, drug effects, Cell Cycle Checkpoints, Cell Proliferation, Cyclooxygenase 2, genetics, metabolism, Cyclooxygenase Inhibitors, pharmacology, Dinoprostone, Down-Regulation, Gene Expression Regulation, Neoplastic, Hep G2 Cells, Humans, Polysaccharides, Reactive Oxygen Species, Triterpenes

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          Abstract

          Cyclooxygenase (COX)-2, a multi-functional molecule, is overexpressed in hepatocellular carcinomas. In order to understand cell proliferation and its association with COX-2 in HepG2 cells in the presence of ursolic acid (UA), viili exopolysaccharides (VEPS) and Astragalus polysaccharides (APS), the cell proliferation, superoxide dismutase (SOD) and metabolic malondialdehyde (MDA) of fatty acids, COX-2, prostaglandin E2 (PGE2), as well as apoptotic morphology and rate were investigated. The results revealed that the activities of SOD, COX-2 and PGE2 were reduced, MDA was markedly decreased, apoptotic blebs were induced, and HepG2 cells were accumulated in the G1 and sub G1/apoptotic phases in test groups. The results indicated that UA, VEPS, APS and any combination of these possess anticancer properties, particularly by downregulating COX-2 expression, which may have increased internal oxidation and triggered apoptosis together with a change in internal antioxidant response elements, leading to a reduction in cell proliferation.

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