AIM： To evaluate role Cadmium （Cd） exposure line Hep3B cells. of midkine secretion during in the human hepatocyte cell METHODS： Different dosages of Cd （0.5-1-5-10 μg/mL） were applied to Hep3B cells and their e...AIM： To evaluate role Cadmium （Cd） exposure line Hep3B cells. of midkine secretion during in the human hepatocyte cell METHODS： Different dosages of Cd （0.5-1-5-10 μg/mL） were applied to Hep3B cells and their effects to apoptosis, lactate dehydrogenase （LDH） leakage and midkine secretion were evaluated as time dependent manner. Same experiments were repeated with exogenously applied midkine （250-5000 pg/mL） and/or 5 t^g/mL Cd. RESULTS： Cd exposure induced prominent apoptosis and LDH leakage beginning from lower dosages at the 48^th. Cd induced midkine secretion with higher dosages （P 〈 0.001）, （control, Cd 0.5-1-5-10μg/mL respectively： 1123 ± 73, 1157 ± 63, 1242 ± 90, 1886 ± 175, 1712 ± 166 pg/mL）. Exogenous 500-5000 pg/mL midkine application during 5 μg/mL Cd toxicity prevented caspase-3 activation （control, Cd toxicity, 250, 500, 1000, 2500, 5000 pg/mL midkine＋ Cd toxicity, respectively： 374 ± 64, 1786 ± 156, 1545 ± 179, 1203 ± 113, 974 ± 116, 646 ± 56, 556 ± 63 cfu） LDH leakage and cell death in Hep3B cells （P 〈 0.001）. CONCLUSION： Our results showed that midkine secretion from Hep3B cells during Cd exposure protects liver cells from Cd induced cellular damage. Midkine has anti-apoptotic and cytoprotective role during Cd toxicity. Further studies are needed to explain the mechanism of midkine secretion and cytoprotective role of midkine during Cd exposure. Midkine may be a promising theurapatic agent in different toxic hepatic diseases.展开更多
基金Supported by TUBITAK- project No. SBAG-2812-104S329
文摘AIM： To evaluate role Cadmium （Cd） exposure line Hep3B cells. of midkine secretion during in the human hepatocyte cell METHODS： Different dosages of Cd （0.5-1-5-10 μg/mL） were applied to Hep3B cells and their effects to apoptosis, lactate dehydrogenase （LDH） leakage and midkine secretion were evaluated as time dependent manner. Same experiments were repeated with exogenously applied midkine （250-5000 pg/mL） and/or 5 t^g/mL Cd. RESULTS： Cd exposure induced prominent apoptosis and LDH leakage beginning from lower dosages at the 48^th. Cd induced midkine secretion with higher dosages （P 〈 0.001）, （control, Cd 0.5-1-5-10μg/mL respectively： 1123 ± 73, 1157 ± 63, 1242 ± 90, 1886 ± 175, 1712 ± 166 pg/mL）. Exogenous 500-5000 pg/mL midkine application during 5 μg/mL Cd toxicity prevented caspase-3 activation （control, Cd toxicity, 250, 500, 1000, 2500, 5000 pg/mL midkine＋ Cd toxicity, respectively： 374 ± 64, 1786 ± 156, 1545 ± 179, 1203 ± 113, 974 ± 116, 646 ± 56, 556 ± 63 cfu） LDH leakage and cell death in Hep3B cells （P 〈 0.001）. CONCLUSION： Our results showed that midkine secretion from Hep3B cells during Cd exposure protects liver cells from Cd induced cellular damage. Midkine has anti-apoptotic and cytoprotective role during Cd toxicity. Further studies are needed to explain the mechanism of midkine secretion and cytoprotective role of midkine during Cd exposure. Midkine may be a promising theurapatic agent in different toxic hepatic diseases.
