ABSTRACT
Objective To investigate the effects of ginsenoside Rb1 pretreatment on the expression of brain derived neurotrophic factor (BDNF) in hippocampus of rat models under acute immobilization stress.Methods Eighteen Sprague-Dawley (SD) rats were randomly divided into three groups (each n =6):normal control group,acute immobilization stress model group,and ginsenoside Rbl group.The rats in acute immobilization stress model group and ginsenoside Rb1 group were exposed to acute immobilization for 2 hours.Thirty minutes before the modeling,ginsnoside Rb1 (40 mg/kg) was injected intraperitoneally into rats in the ginsenoside Rbl group,and the control group was not treated.The enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of plasma cortisol (CORT) and adrenocorticotropic hormone (ACTH).The real-time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-PCR) was applied to examine the expression of BDNF mRNA in rat hippocampus and its expression of BDNF protein was measured by Western Blot.Results In acute immobilization stress model group,compared with those before modeling,the plasma CORT and ACTH concentrations were significantly higher after modeling [CORT (μg/L):3.79 ± 0.50 vs.2.06 ± 0.35,ACTH (μg/L):1.69 ± 0.12 vs.0.94 ± 0.12,both P ＜0.05];compared with the normal control group,the mRNA and protein expressions of BDNF in hippocampus in the acute immobilization stress model group were decreased significantly [BDNF mRNA (A value):42.87 ± 5.56 vs.109.39 ± 9.11,BDNF protein (grey value):0.94 ± 0.02 vs.1.02 ± 0.03,both P ＜ 0.01];compared with acute immobilization stress model group,the mRNA (113.73 ± 6.24 vs.42.87 ± 5.56) and protein expressions (1.04 ± 0.02 vs.0.94 ± 0.02) of BDNF in hippocampus of pre-treatment groups were significantly higher (all P ＜ 0.05).Conclusions The results suggest that pretreatment with ginsenoside Rb1 alleviate hippocampus lesion induced by acute immobilization stress through regulating the BDNF mRNA and protein expressions in hippocampus.
ABSTRACT
Background: Exposure to stress-factors caused an array of biochemical, physiological and behavioral changes. According to literature data, specific stressors may elicit specific responses, and different stressors may activate different brain systems by using specific pathways within the central nervous system. Several brain structures, including the periaqueductal gray (PAG), have been implicated in the functional neuroanatomy of stress response. The dorsolateral column of the periaqueductal gray (dlPAG) integrates aversive emotional experiences and represents an important site responding to life threatening situations. It was reported that nitric oxide (NO) affects the neuronal activity of the PAG. The goal of the present study was to investigate the changes of NO activity in the dlPAG of immobilized rats using a histochemical examination of the distribution of NADPH-d reactivity neurons. Our results showed that NO activity in rat’s dlPAG was significantly increased by acute immobilization stress. This suggests a pivotal role of this part of the brain and NO-ergic system in stress response which main role is to attenuate the effect of stress and to restore the homeostasis. Methods: The experiments were carried out on male Wistar rats (180-200g), divided into two groups. The first group represented intact controls. The second group was subjected to acute immobilization stress. Results: The acute stressor – 1 hour immobilization, showed statistically significant increase in the number of the NADPH-d positive neurons compared to the control group (p < 0.01). Conclusion: NO activity in rat’s dlPAG was significantly increased by acute immobilization stress.
ABSTRACT
PURPOSE: Many stresses produce reactive oxygen species and bring about mechanism of antioxidant reaction. Cytokine and a neurotransmitter through the cell membrane, as well as signal transduction through the cell membrane, are used for various pathological condition of the brain, such as neurodegenerative disease. There are several antioxidant enzymes in cells (superoxcide dismutase, glutathion peroxidasae, peroxiredoxin catalase, etc.) METHODS: This study used single- or double-label immunohistochemical techniques to analyze mouse spinal neuron cells expressing Prx I and Prx III after acute mobilization stress. RESULTS: Prx I was observed in dendritic cell of the gray matter of the spinal cord, and Prx III was observed in the cytoplasm of the GM of the spinal cord. CONCLUSION: The results of this study will help to explain differences of expression in the distributions of the peroxiredoxin enzymes of the spinal cord.
Subject(s)
Animals , Mice , Brain , Catalase , Cell Membrane , Cytoplasm , Dendritic Cells , Immobilization , Neurodegenerative Diseases , Neurons , Neurotransmitter Agents , Peroxiredoxins , Reactive Oxygen Species , Signal Transduction , Spinal CordABSTRACT
PURPOSE: Many stresses produce reactive oxygen species and bring about mechanism of antioxidant reaction. Cytokine and a neurotransmitter through the cell membrane, as well as signal transduction through the cell membrane, are used for various pathological condition of the brain, such as neurodegenerative disease. There are several antioxidant enzymes in cells (superoxcide dismutase, glutathion peroxidasae, peroxiredoxin catalase, etc.) METHODS: This study used single- or double-label immunohistochemical techniques to analyze mouse spinal neuron cells expressing Prx I and Prx III after acute mobilization stress. RESULTS: Prx I was observed in dendritic cell of the gray matter of the spinal cord, and Prx III was observed in the cytoplasm of the GM of the spinal cord. CONCLUSION: The results of this study will help to explain differences of expression in the distributions of the peroxiredoxin enzymes of the spinal cord.