• Journal of Nutrition and Health
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• v.14 no.2
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• pp.105-116
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• 1981

A quantitative restriction of maternal diet without changes in quality of diet was given to the Sprague Dawley rats during the third week of gestation and lactation. Half the normal average daily intake of control group was given to deficient groups in this period. Female rats of control group were fed a commercial diet ad libitum throughout the experimental period. Dietary restriction started from birth to weaning in deficient I group and from the 15th day of gestation to weaning in deficient II group. Body and brain weight of offsprings of deficient groups were significantly lower than control group, but the ratios of brain weight to body weight in deficient groups were higher than the control group. Significant difference between deficient groups (I and II) was noticed at weaning. Brain DNA, RNA and total protein of offsprings of deficient groups were significantly lower than control group, but RNA/DNA, brain weight/DNA, and total protein/DNA show that cell number were more affected than the cell size by the maternal dietary restriction during the third week of gestation and lactation. Between the deficient groups, there was a significant difference in brain DNA and RNA, but no significant difference in total brain protein. (This research was supported in part by grant from the Ministry of Education.)

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.6
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• pp.1643-1651
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• 2004

This experimental study was designed to investigate the effects of SIEGESBECKIAE HERBA extract (SHE) on the change of cerebral hemodynamics 〔regional cerebral blood flow (rCBF) and mean arterial blood pressure(MABP)〕 in normal condition and cerebral ischemic rats, and to determine the mechanism of action of SHE. This study was designed to investigate whether or not SHE inhibit lactate dehydrogenase (LDH) activity in neuronal cells and cytokines production in serum of cerebral ischemic rats. The results were as follows SHE increased rCBF significantly in a dose-dependent manner, but MABP was not changed by SHE in normal rats. The SHE-induced increase in rCBF was significantly inhibited by pretreatment with indomethacin (IDN), an inhibitor of cyclooxygenase but was increased by methylene blue (MTB), an inhibitor of guanylate cyclase. SHE inhibited lactate dehydrogenase (LDH) activity significantly in neuronal cells. rCBF was increased significantly and stably by SHE(10㎎/㎏, i.p.) during the period of cerebral reperfusion, which contrasted with the findings of rapid and marked increase in control group in ischemic rats. In serum by drawing from femoral arterial blood after middle cerebral arterial occlusion(MCAO) for 1hr and reperfusion for 1hr, the sample group was decreased IL-1β production significantly compared to that of the control group. In serum by drawing from femoral arterial blood after MCAO 1hr and reperfusion 1hr, sample group decreased TNF-α production significantly compared to that of the control grolilp. In serum by drawing from femoral arterial blood after reperfusion 1hr, sample group increased TGF-β production significantly compared to that of the control group. In serum by drawing from femoral arterial blood after MCAO for 1hr and reperfusion for 1hr, IL-10 production of the sample group was similar to that of control group. These results suggested that SHE had inhibitive effect on the brain damage by inhibited LDH activity, IL-1β and TNF-α production, but accelerated TGF-β production.

• Korean Journal of Oriental Medicine
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• v.9 no.1
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• pp.157-178
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• 2003

Objective : This study was designed to assess the protective effects of Chengwhabosimtang on the animal model of depression, chronic mild stress(CMS). Method : Male Sprague-Dawley rats Were used for this experiment. The subjects Were divided into 3 groups (1. CMS-drug: Chengwhabosimtang administered during CMS treatment, 2. CMS-vehicle: water administered, 3. normal ). After 4 weeks of CMS treatment they were executed Forced swimming test(FST) and Elevated plus maze. Tyrosine hydroxylase(TH) in ventral tegmental area(VTA) and c-Fos in paraventricular nucleus(PVN) were measured. Result : 1. In FST, CMS-drug group showed significantly decreased immobility behavior. 2. CMS-drug group showed no significantly lower TH level in VTA than CMS-vehicle group. 3. CMS-drug group showed significantly less c-Fos expressed cell bodies in PVN than CMS-vehicle group. 4. In Elevated plus maze, CMS-drug group showed no significantly anxiety. Conclusion : These results suggest that Chengwhabosimtang may have protective antidepressant effects in CMS model rats. And these effects could be explained by the elevated stress-copying behaviors which are related with PVN of hypothalamus and dopaminergic neurons in VTA.

• Physical Therapy Korea
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• v.16 no.2
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• pp.41-49
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• 2009

This study was designed to investigate the effects of treadmill exercise of low-intensity and moderate- intensity on the functional recovery and histological change in spinal cord injury (SCI) rats. SCI was induced by the spinal cord impactor dropped after laminectomy. Experimental groups were divided into the Group I (normal control), Group II (non-treatment after SCI induction), Group III (low-intensity treadmill exercise after SCI induction), Group IV (moderate-intensity treadmill exercise after SCI induction). After operation, rats were tested at modified Tarlov scale at 2 days with divided into 4 groups, and motor behavior test (BBB locomotor rating scale, Grid walk test) was examined at 3, 7, 14, and 21 days. For the observation of damage change and size of the organized surface in spinal cord, histopathological studies were performed at 21 days by H & E, and BDNF(brain-derived neutrophic factor) & Trk-b immunohistochemistry studies were performed at 1, 3, 7, 14, 21 days. According to the results, treadmill exercise can play a role in facilitating recovery of locomotion following spinal cord injury. Specially, moderate-intensity treadmill exercise after SCI induction was most improvement in functional recovery and histological change.

• The Korean Journal of Pain
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• v.25 no.4
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• pp.228-237
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• 2012

Background: Milnacipran is a balanced serotonin norepinephrine reuptake inhibitor with minimal side effects and broad safety margin. It acts primarily on the descending inhibitory pain pathway in brain and spinal cord. In many animal studies, intrathecal administration of milnacipran is effective in neuropathic pain management. However, there is no study for the neurological safety of milnacipran when it is administered neuraxially. This study examined the neurotoxicity of epidural milnacipran by observing behavioral and sensory-motor changes with histopathological examinations of spinal cords in rats. Methods: Sixty rats were divided into 3 groups, with each group receiving epidural administration of either 0.3 ml (3 mg) of milnacipran (group M, n = 20), 0.3 ml of 40% alcohol (group A, n = 20), or 0.3 ml of normal saline (group S, n = 20). Results: There were no abnormal changes in the behavioral, sensory-motor, or histopathological findings in all rats of groups M and S over a 3-week observation period, whereas all rats in group A had abnormal changes. Conclusions: Based on these findings, the direct epidural administration of milnacipran in rats did not present any evidence of neurotoxicity in behavioral, sensory-motor and histopathological evaluations.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.1
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• pp.75-83
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• 2004

This experimental study was designed to investigate the effects of Sagunja-tang(SGJT), Ijin-tang(IJT), Yukgunja-tang(YGJT) on the change of cerebral hemodynamics [regional cerebral blood f1ow(rCBF), mean arterial blood pressure(MABP), and pial arterial diameter (PAD)] in normal rats, and further to determine the mechanism of action of YGJT. And, this Study was designed to investigate whether YGJT inhibit lactate dehydrogenase(LDH) activity in neuronal cells. The results were as follows ; 1. SGJT significantly increased rCBF but MABP was not changed comparing with normal MABP(l00 %). This results were suggested that SGJT significantly increased rCBF by dilating PAD. 2. IJT significantly decreased rCBF in a dose-dependent, but significantly increased MABP in a dose-dependent. This results were suggested that IJT significantly decreased rCBF by contracting PAD. 3. YGJT significantly increased rCBF and PAD in a dose-dependent, and YGJT increased MABP compared with normal MABP(100 %). This results were suggested that YGJT significantly increased rCBF by dilating PAD. 4. The YGJT-induced increase in rCBF was significantly accelerated by pretreatment with indomethacin (IDN, 1 mg/kg, i.p.), an inhibitor of cyclooxygenase but was significantly inhibited by methylene blue (MTB, 10 ㎍/㎏ i.p.), an inhibitor of guanylate cyclase. 5. The YGJT-induced increase in PAD and MABP were accelerated by pretreatment with IDN but was significantly inhibited by MTB. This results suggested that the mechanism of YGJT is mediated by guanylate cyclase. 6. YGJT inhibited significantly LDH activity in neuronal cells. This results were suggested that YGJT prevented the neuronal death. I thought that YGJT should have improvement of cerebral hemodynamics and inhibitive effect on the brain damage.

• Biomedical Science Letters
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• v.29 no.4
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• pp.263-273
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• 2023

This study aimed to investigate effect of scalp acupuncture (SA) and repetitive transcranial magnetic stimulation (rTMS) intervention on neuromotor function in photothrombotic cerebral infarction (PCI) rat model. Sixty male SD rats were used. PCI was induced on M1 cortex of right frontal lobe. SA was performed at the Qianding (GV21), Xuanli (GB6) acupoints of ipsilesional M1. Low-frequency rTMS was delivered to contralesional M1. All rats were randomly divided into 4 groups: group A, normal (n, 15); group B, PCI without any stimulation intervention (n, 15); group C, PCI with SA (n, 15); group D, PCI with rTMS (n, 15). Rota-rod test and Ladder rung walking test (LWT) were done weekly for 8 weeks after PCI. SA or rTMS was started from post-PCI 4^th day as protocol for 8 weeks. H/E stain and IHC were done. Western blot and qRT-PCR study were performed for MAP2 and BDNF from ipsilesional M1 peri-infarction tissue. Brain MRI study was conducted to quantify the volume of cerebral infarction. As a result, left forelimb and hindlimb function significantly improved more in group C and D than control group, with expressed more BDNF and MAP2. And brain MRI showed focal infarction of right M1 after PCI, and infarction volume progressively decreased in group C and D than group B from post-PCI 5^th to 8^th week. SA or rTMS was more effective than no intervention group on neuromotor function of PCI rat model. The functional recovery was associated with stimulation intervention-related neurogenesis.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.2
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• pp.117-125
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• 1997

The N-methyl-D-aspartate (NMDA) receptor-mediated glutamatergic neurotransmission is involved in synaptic plasticity, developmental processes, learning and memory and many neuropathological disorders including age-related diseases. In the present study, regulation of the NMDA receptor properties by various ligands was investigated using $[^3H]MK-801$ binding studies in the synaptic membranes of young and aged rat forebrains. The binding in the presence of glutamate and glycine increased dramatically with growth between 1 and 6 weeks old, and thereafter declined gradually with aging. Glutamate, glycine or spermine respectively increased the binding with growth. Glutamate maintained the binding during aging, while glycine or spermine significantly decreased the binding in the aged brain. The maximum stimulation by glycine varied depending on the ages of brains. Greater sensitivity to glycine was observed at 1 week and 3 months and the sensitivity was significantly reduced in the aged brain. In contrast, spermine showed similar stimulation patterns in young and aged rats. These results indicated that the functional properties of the NMDA receptor-ion channel complex in young and aged rat forebrains are differentially regulated by agonists, and the reduction of the receptor function with normal aging may be, in some degree, due to the reduction of the receptor sensitivity to glycine.

• Journal of Korean Biological Nursing Science
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• v.24 no.2
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• pp.77-85
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• 2022

Purpose: Aging process comes with cognitive impairment due to decreased neuronal cell number, activity, and neuronal circuit. Alteration of inhibitory neurons contributes to cognitive impairment in normal aging and is responsible for disrupting the excitation/inhibition balance by reducing the synthesis of gamma-aminobutyric acid (GABA). Morus nigra (Mulberry) is a natural physiologically active substance that has been proven to have anti-oxidant, anti-diabetic, and anti-inflammatory effects through many studies. This study aimed to evaluate the effects of the mulberry extract (ME) on cognitive function through anti-oxidant enzyme and GABAergic neuronal activity in aged rat brain. Methods: Sprague Dawley rats were randomly assigned as the young group (8 weeks, n= 8), aging group (67 weeks, n= 8), and aging+ mulberry extract group (67 weeks, n= 8). The aging+ mulberry extract group was orally administered 500 mg/kg/d mulberry extract for 6 weeks. Results: The aging+ mulberry extract group improved spatial and short-term memory. The antioxidant potential of ME increased the expression of superoxide dismutase-1 (SOD-1) and decreased inducible nitric oxide synthase (iNOS). Also, the aging+ mulberry extract group significantly increased the expression of GABAergic interneuron in hippocampus cornu ammonis1 (CA1) compared to the aging group. Conclusion: The number of GABAergic inhibitory interneurons was deceased and memory functions in the aging process, but those symptoms were improved and restored by mulberry extract administration.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.6
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• pp.1546-1551
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• 2005

This Study was designed to investigate the effects of Nelumbinis Rhizomatis Nodus (NRN) on the change of cerebral hemodynamics [regional cerebral blood flow (rCBF), pial arterial diameter (PAD) and mean arterial blood pressure (MABP)] in normal and cerebral ischemic rats. And, this study was designed to investigate the inhibition of lactate dehydrogenase activity in neuronal cells The results were as follows NRN significantly increased rCBF and PAD in a dose-dependent manner, and NRN increased MABP in a dose-dependent manner. This results suggested that NRN significantly increased rCBF by dilating PAD. Both rCBF and PAD were significantly and stably increased by NRN (10 mg/kg, i.p.) during the period of cerebral reperfusion, which contrasted with the findings of rapid and marked increase in control group. NRN significantly inhibited lactate dehydrogenase activity in neuronal cells. This results suggested that NRN prevented the neuronal death. It is suggested that NRN had an anti-ischemic effect through the improvement of cerebral hemodynamics and inhibitive effect on the brain damage.