AIM： To evaluate the effects of betaine on the ethanolinduced secretion of IGF-I and IGFBP-1 using radioimrnunoassay and Western blotting, respectively, in primary cultured rat hepatocytes. METHODS： Hepatocytes isol...AIM： To evaluate the effects of betaine on the ethanolinduced secretion of IGF-I and IGFBP-1 using radioimrnunoassay and Western blotting, respectively, in primary cultured rat hepatocytes. METHODS： Hepatocytes isolated from male SpragueDawley rats were incubated with various concentrations of ethanol and PD98059 procedures. The hepatocytes were also treated with different doses of betaine （10^-5, 10^-4, and 10^-3 mol/L）. We measured IGF-I and IGFBP-1 using radioimmunoassay and Western blotting, respectively. RESULTS： The ethanol-induced inhibition of IGF-I secretion was attenuated by betaine in a concentration-dependent manner in primary cultured rat hepatocytes. At 10^-3 mol/L, betaine significantly increased IGF-I secretion but decreased IGFBP-1 secretion. In addition, p42/44 rnitogen-activated protein kinase （MAPK） activity was accelerated significantly from 10 min to 5 h after treatment with 10^-3 mol/L betaine. Furthermore, the changes in IGF-1 and IGFBP-1 secretion resulting from the increased betaine-induced p42/44 MAPK activity in primary cultured rat hepatocytes was blocked by treatment with the MAPK inhibitor PD98059. Betaine treatment blocked the ethanol-induced inhibition of IGF-I secretion and p42/44 MAPK activity, and the ethanol-induced increase in IGFBP-1 secretion.CONCLUSION： Betaine modulates the secretion of IGF-I and IGFBP-1 via the activation of p42144 MAPK in primary cultured rat hepatocytes. Betaine also alters the MAPK activations induced by ethanol.展开更多
Danshen has been used in stroke treatment for thousands of years in China. However, the underlying mechanism still remains elusive. Neuron loss is the cardinal feature of stroke. Stimulating endogenous neurogene- sis,...Danshen has been used in stroke treatment for thousands of years in China. However, the underlying mechanism still remains elusive. Neuron loss is the cardinal feature of stroke. Stimulating endogenous neurogene- sis, especially neuronal differentiation, might potentially provide therapeutic effects to these diseases. To interpret Danshen＇ s disease-modifying effects, the effects of tanshinone 11 A （T 11 A）, the major lipophilic component of Danshen, on neuronal differentiation in rat PC12 pheochromocytoma cells and the rat embryonic cortical neural stem cells （NSCs） were observed. PC12 cells and NSCs were incubated with T II A for 7 days. To detect the neu- ronal differentiation, GAP-43 expression was detected by western blots assay and β-tubulin HI expression was de- tected by immunocytochemical staining. Results showed that T Ⅱ A dose-dependently promoted neuronal differentia- tion. T Ⅱ A activated mitogen-activated protein kinase 42/44 （MAPK42/44） and its downstream transcription fac- tor, cAMP response element-binding protein （CREB）. In addition , T Ⅱ A up-regulated the expressions of brain de- rived neurotrophic factor （BDNF） and nerve growth factor （NGF）. The MEK inhibitor and the antagonist to the re- ceptors of NGF and BDNF could partially attenuate the differentiation effects, indicating that MAPK42/44 mediated BDNF and NGF signals were involved in T Ⅱ A＇ s differentiation effects. Caveolin-1 （ CAV-1 ）, the major functional protein of membrane caveolae, plays critical roles in the endocytosis of exogenous materials. CAV1, which was ac-tivated by T Ⅱ A, might help T Ⅱ A transport across cell membrane to initiate its differentiation effects. It was prov- en by the evidences that suppressing the function of caveolin inhibited the differentiation effects of T Ⅱ A. There- fore, it was concluded that T Ⅱ A promoted neuronal differentiation partially through MAPK42/44 mediated B DNF and NEF signals in a caveolae-dependent manner.展开更多
文摘AIM： To evaluate the effects of betaine on the ethanolinduced secretion of IGF-I and IGFBP-1 using radioimrnunoassay and Western blotting, respectively, in primary cultured rat hepatocytes. METHODS： Hepatocytes isolated from male SpragueDawley rats were incubated with various concentrations of ethanol and PD98059 procedures. The hepatocytes were also treated with different doses of betaine （10^-5, 10^-4, and 10^-3 mol/L）. We measured IGF-I and IGFBP-1 using radioimmunoassay and Western blotting, respectively. RESULTS： The ethanol-induced inhibition of IGF-I secretion was attenuated by betaine in a concentration-dependent manner in primary cultured rat hepatocytes. At 10^-3 mol/L, betaine significantly increased IGF-I secretion but decreased IGFBP-1 secretion. In addition, p42/44 rnitogen-activated protein kinase （MAPK） activity was accelerated significantly from 10 min to 5 h after treatment with 10^-3 mol/L betaine. Furthermore, the changes in IGF-1 and IGFBP-1 secretion resulting from the increased betaine-induced p42/44 MAPK activity in primary cultured rat hepatocytes was blocked by treatment with the MAPK inhibitor PD98059. Betaine treatment blocked the ethanol-induced inhibition of IGF-I secretion and p42/44 MAPK activity, and the ethanol-induced increase in IGFBP-1 secretion.CONCLUSION： Betaine modulates the secretion of IGF-I and IGFBP-1 via the activation of p42144 MAPK in primary cultured rat hepatocytes. Betaine also alters the MAPK activations induced by ethanol.
文摘Danshen has been used in stroke treatment for thousands of years in China. However, the underlying mechanism still remains elusive. Neuron loss is the cardinal feature of stroke. Stimulating endogenous neurogene- sis, especially neuronal differentiation, might potentially provide therapeutic effects to these diseases. To interpret Danshen＇ s disease-modifying effects, the effects of tanshinone 11 A （T 11 A）, the major lipophilic component of Danshen, on neuronal differentiation in rat PC12 pheochromocytoma cells and the rat embryonic cortical neural stem cells （NSCs） were observed. PC12 cells and NSCs were incubated with T II A for 7 days. To detect the neu- ronal differentiation, GAP-43 expression was detected by western blots assay and β-tubulin HI expression was de- tected by immunocytochemical staining. Results showed that T Ⅱ A dose-dependently promoted neuronal differentia- tion. T Ⅱ A activated mitogen-activated protein kinase 42/44 （MAPK42/44） and its downstream transcription fac- tor, cAMP response element-binding protein （CREB）. In addition , T Ⅱ A up-regulated the expressions of brain de- rived neurotrophic factor （BDNF） and nerve growth factor （NGF）. The MEK inhibitor and the antagonist to the re- ceptors of NGF and BDNF could partially attenuate the differentiation effects, indicating that MAPK42/44 mediated BDNF and NGF signals were involved in T Ⅱ A＇ s differentiation effects. Caveolin-1 （ CAV-1 ）, the major functional protein of membrane caveolae, plays critical roles in the endocytosis of exogenous materials. CAV1, which was ac-tivated by T Ⅱ A, might help T Ⅱ A transport across cell membrane to initiate its differentiation effects. It was prov- en by the evidences that suppressing the function of caveolin inhibited the differentiation effects of T Ⅱ A. There- fore, it was concluded that T Ⅱ A promoted neuronal differentiation partially through MAPK42/44 mediated B DNF and NEF signals in a caveolae-dependent manner.
