Xueyuan Jin1, Tao Cong2, Lin Zhao3, Long Ma4, Reisheng Li5, Ping Zhao1, Changjiang Guo2. 1. International Center for Liver Disease Treatment, 302 Hospital Beijing 10039, China. 2. Institute of Health and Environmental Medicine Tianjin 30050, China. 3. Department of Nutrition, General Hospital of P.L.A Beijing 100853, China. 4. The Second Artillery General Hospital of P.L.A Beijing 100082, China. 5. Animal Center, Beijing 302 Hospital Beijing 100039, China.
Abstract
OBJECTIVE: We observed the effects of Masson pine pollen aqueous extracts (MPPAE) on CCl4-induced oxidative damage of the human hepatic cell line L-02. METHODS: We created an in vitro model of oxidative liver damage by treating L-02 human hepatic cells with 40 mmol/L CCl4. Effects of different concentrations of MPPAE on cell proliferation, morphology, and change of functional indexes were observed after addition of CCl4. RESULTS: CCl4 was toxic to proliferation, cell morphology, and functionality of hepatic cells. It decreased proliferation by 29.3-38.4% and increased AST and ALT activities by 22.3% and 99.2%, respectively. The oxidative stress also disrupted hepatic cell growth and induced pyknosis. Although MPPAE did not prevent decreased proliferation of L-02 cells, the treatment alleviated some CCl4-induced cell morphology changes and inhibited the abnormal rise of ALT (39.8%-70.1%) and AST (14.75-27.25%) activities in a dose dependent manner. A high dose of MPPAE (400 mg/L) ameliorated nucleus deformation to an almost normal appearance. CONCLUSIONS: According to our in vitro model, MPPAE specifically prevented the changes in cell morphology and functional injury caused by CCL4 treatment; however, it offered limited protection against damage-induced reduction of proliferation.
OBJECTIVE: We observed the effects of Masson pine pollen aqueous extracts (MPPAE) on CCl4-induced oxidative damage of the human hepatic cell line L-02. METHODS: We created an in vitro model of oxidative liver damage by treating L-02 human hepatic cells with 40 mmol/L CCl4. Effects of different concentrations of MPPAE on cell proliferation, morphology, and change of functional indexes were observed after addition of CCl4. RESULTS:CCl4 was toxic to proliferation, cell morphology, and functionality of hepatic cells. It decreased proliferation by 29.3-38.4% and increased AST and ALT activities by 22.3% and 99.2%, respectively. The oxidative stress also disrupted hepatic cell growth and induced pyknosis. Although MPPAE did not prevent decreased proliferation of L-02 cells, the treatment alleviated some CCl4-induced cell morphology changes and inhibited the abnormal rise of ALT (39.8%-70.1%) and AST (14.75-27.25%) activities in a dose dependent manner. A high dose of MPPAE (400 mg/L) ameliorated nucleus deformation to an almost normal appearance. CONCLUSIONS: According to our in vitro model, MPPAE specifically prevented the changes in cell morphology and functional injury caused by CCL4 treatment; however, it offered limited protection against damage-induced reduction of proliferation.
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