Antithrombin III stimulates prostaglandin I2 production by cultured rat hepatic sinusoidal endothelial cells |
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| Affiliation: | 1. Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan;2. Department of Neurology, Kurashiki Heisei Hospital, Okayama, Japan;3. Department of Pediatrics and Developmental Biology, Tokyo Medical and Dental University, Tokyo, Japan;1. Department of Neurology, Affiliated Hospital of Jining Medical College, Jining, Shandong Province, PR China;2. Central Laboratory, Affiliated Hospital of Jining Medical College, Jining, Shandong Province, PR China;3. Department of Haemotology, Affiliated Hospital of Jining Medical College, Jining, Shandong Province, PR China;4. Department of Neurology, Affiliated Hospital of Xuzhou Medical College, Xuzhou, Jiangsu Province, PR China;5. Departments of Medicine and Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore |
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| Abstract: | We examined the production of prostanoids, specifically prostaglandin (PG) I2 and thromboxane (TX) A2, in cultured rat hepatic sinusoidal endothelial cells treated with antithrombin (AT) III. When cells were treated for 3 h with various concentration of AT III, production of 6-keto-PGF1α (a stable metabolite of PG I2) increased significantly and in a dose-dependent manner, compared with production by untreated cells. In terms of kinetics, significant increases were noted at 3 h (20.13 ± 1.38 pg/ml), 4 h (21.23 ± 0.63 pg/ml) and 24 h (36.58 ± 4.93 pg/ml) with AT III (300 μg/ml) stimulation, compared with production by the untreated cells (10.29 ± 1.21, 10.34 ± 1.66 and 22.64 ± 2.59 pg/ml, respectively). Moreover, this production was significantly reduced with increasing concentrations of heparin. On the other hand, TX B2 (a stable metabolite of TX A2) production was unaffected by AT III treatment. These data suggest that AT III may ameliorate the liver damage or disturbances in the sinusoidal microcirculation by stimulating the PG I2 production of hepatic sinusoidal endothelial cells. |
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