ABSTRACT
@#ObjectiveTo observe the changes of monoamine oxidase-B (MAO-B), interleukin-6(IL-6) in the cortex and hippocampus of Alzheimer's disease model mice and the effect of traditional Chinese medicine Naofucong.MethodsAlzheimer's disease model was induced in mice by β-amyloid(Aβ)25-35 icv. Space learning and memorial ability was tested in Morris water maze. The activity of MAO-B was measured by colorimetric method. IL-6 was observed with the immnuohistochemical stain.ResultsMice in the model group presented longer latent periods of Morris water maze(81.3±13.4)s, higher activities of MAO-B in brain cortex and hippocampus (120.12±10.15,83.60±5.29) compare with that of the control group, which was (34.2±10.9)s,(93.09±10.54) and (50.39±9.16)(P<0.05～0.01).There were many IL-6 positive cell in dentate gyrus of hippocampus of the model group. After administration with Naofucong grain, latent periods (43.7±12.7) s and activities of MAO-B (47.11 ± 6.57)in hippocampus were recovered(P<0.05～0.01), and the IL-6 positive cell in dentate gyrus decreased.ConclusionNaofucong grain can antagonize the Aβ25-35 toxicity by decreasing the overactivition of MAO-B and the excretion of inflammatory medium by microglia, as well as improve the memory function.
ABSTRACT
This study was designed to investigate the effects of buthanol (BuOH) fraction of pine (Pinus densiflora Sieb et Zucc) needle on cholesterol and lipofuscin (LF) accumulations, acetylcholine (ACh) and its related enzyme activities such as choline acetyltransferase (CAhT) and acetylcholinesterase (AChE), and monoamone oxidase-B (MAO-B) activity, which destroyed the catecholamine-related neurotransmitters in brain membranes of Sprague-Dawley (SD) rats. Male SD rats were fed basic diets (control group) or experimental diets (BuOH-25, BuOH-50 and BuOH-100) for 45 days. Cholesterol accumulations in mitochondria and microsomes were significantly inhibited (about 14 - 17% and 23 - 34%, respectvely) in BuOH-50 and BuOH-100 groups, whereas LF levels were significantly inhibited (about 10 - 14%) in BuOH-50 and BuOH-100 groups compared with control group. ACh levels and ChAT activities were significantly increased (about 11 - 17% and 11 - 23%, respectively) in membranes of BuOH-50 and BuOH-100 groups compared with control group. AChE activities were significantly increased (about 14 - 17%) in membranes of BuOH-50 and BuOH-100 groups. There was no significant difference in MAO-B activities between control and experimental diet groups. The results suggest that butanol fraction of pine needle may play an effective role in an antiaging effect and improving a learning and memory impairments.
Subject(s)
Animals , Humans , Male , Rats , Acetylcholine , Acetylcholinesterase , Brain , Cholesterol , Choline O-Acetyltransferase , Diet , Learning , Lipofuscin , Membranes , Memory , Microsomes , Mitochondria , Monoamine Oxidase , Needles , Neurotransmitter Agents , Rats, Sprague-DawleyABSTRACT
Object To study the effects of total alkaloids in Equisetum pratense Ehrh. (TAEP) on the activity of monoamine oxidase B (MAO B) in mice brain, to reveal the mechanism of its inhibitory action on the central nervous system (CNS). Methods The activity of MAO B was determined by UV spectrophotometry. Results TAEP can markedly activate MAO B in cerebrum and antagonise the inhibition of MAO B activity by nialamide. Conclusion TAEP is a MAO B agonist with an action for the evacuation of monoamine, this may be considered as one of the mechanisms of TAEP sedative and tranquilizing action on CNS.
ABSTRACT
Objective:To adopt the brain lesion model of mouse induced by overload aluminum to study the relationship between monoamine oxidase B disorder and neurodegeneration induced by overload aluminum(Al).Method:Aluminum overload models were established by injection of 3?l AlCl3 into lateral ventricle of miceeach day for 5d.The AlCl3 solutions injected in different modelswere with different concentrations and they were 0.125%,0.25%,0.5%.On d10,d20,and d30 after the final administration of AlCl3 solution,the learning and memory function of mice,pathomorphology of hippocampi,and MAO-B activity were determined.Results:Aluminum overload elevated MAO-B activity,caused karyopyknosis and loss of neurons in CA1 area of hippocampi,in dose-and time-dependent manners.Conclusion:The results indicate that neurodegeneration induced by Al toxicity may be related to the monoamine oxidase B homeostasis interfered by Al overload.