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1.
Journal of Central South University(Medical Sciences) ; (12): 840-846, 2010.
Artigo em Chinês | WPRIM | ID: wpr-814386

RESUMO

OBJECTIVE@#To explore the effect of tanshinone IIA (TanIIA) on calcium current induced by beta-amyloid protein 25-35 (Abeta25-35) in neurons of nucleus basalis of Meynert (nbM).@*METHODS@#Cell acute dissociated technique and the whole-cell recording model of patch-clamp technique of single-cell were used. The voltage-dependent calcium current in neurons of nbM was recorded in SD rats first. Then the effect of TanIIA on the voltage-dependent calcium current in the neurons was assayed. The change of calcium current induced by Abeta25-35 as well as the effect of TanIIA on the change of calcium current induced by Abeta25-35 in neurons of nbM were analyzed.@*RESULTS@#Extracellular fluid containing different concentrations of TanIIA was irrigated, respectively. The peak current did not change obviously. There was no difference in current density between the TanIIA group and the control group at 0 mV (P>0.05). Extracellular fluid containing 200 nmol/L Abeta25-35 was irrigated after the normal calcium current recorded under whole patch clamp, and the peak current changed obviously. There was distinct difference in the current density between the Abeta group and the control group at 0 mV (P0.05).@*CONCLUSION@#In vitro, TanIIA could inhibit the calcium current amplification induced by Abeta25-35 in neurons of nbM. TanIIA may protect neurons against the toxicity of Abeta and decrease the inward flow of Ca(2+).


Assuntos
Animais , Feminino , Masculino , Ratos , Abietanos , Farmacologia , Peptídeos beta-Amiloides , Toxicidade , Núcleo Basal de Meynert , Biologia Celular , Metabolismo , Cálcio , Metabolismo , Canais de Cálcio , Células Cultivadas , Medicamentos de Ervas Chinesas , Farmacologia , Neurônios , Biologia Celular , Metabolismo , Fármacos Neuroprotetores , Farmacologia , Técnicas de Patch-Clamp , Fragmentos de Peptídeos , Toxicidade
2.
Journal of Pharmaceutical Analysis ; (6): 116-117,154, 2000.
Artigo em Chinês | WPRIM | ID: wpr-625040

RESUMO

Objective To observe the effects of methionine enkephalin (M-Enk) on migration of macrophages from mice with impaired liver and its immunomodulatory mechanisms. MethodsLiver of mice was impaired by feeding CCl4 and macrophage migration inhibitory factor (MMIF) was produced by Con A-stimulated spleen lympho- cytes. Inhibition of macrophage migration was measured in reaction system by adding M-Enk. Results Migration of macrophages in both liver-impaired and control group were suppressed by MMIF, but the suppression might be re- versed by adding 1 μmol/L M-Enk (P<0. 05). M-Enk could significantly inhibit in vitro both of the combination of MMIF with macrophages and production of MMIF from lymphocytes (P<0. 01). Macrophages from liver-imparied group showed a higher sensitivity compared to the control group (P<0. 05). ConclusionThe study suggests that opi- oid peptieds play an important role in the modulation of the immune response under stress as liver impairment.

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