Journal of Physiology & Pathology in Korean Medicine
/
v.16
no.5
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pp.967-975
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2002
This study was to investigate the metal accumulation from Ohjeoksan-Decoction to rat brain(Sprague Dawley). 1. In Control group, each metal concentration was within 26.65mg/kg, and in each experimental groups, was within 28.39mg/kg. And, there were no significant metal concentration between control and experimental groups. Exceptionally, Cr and Ni level of control group was lower than experimental groups significantly. (p<0.05) and Cr and Ni level of experimental I group was lower than other experimental groups too.(p<0.05). But, Pb level of control group was higher than experimental groups significantly.(p<0.05) Pb level of experimental I group was higher than other experimental groups(p<0.01). 2. In non-hazardous, hazardous and total metal concentration, there was no increase tendency in brain according to the high dose of OD(Ohjeoksan-Decoction) intake. Reversely, in experimental groups, hazardous metal concentration was decrease by high OD intake.(p<0.05). 3. Correlation among each metal in brain was various in each groups. Briefly under the intake of Ohjeoksan-Decoction, that is very busy herb prescription, this study was defined within safety in brain metal level by P.O. during 10 days. But, there should be a more research about Pb increase by high dose OD intake
This study was to investigate the metal accumulation from Ohjeoksan-Decoction to rat brain(Sprague Dawley). 1. In Control group, each metal concentration was within 26.65mg/kg. and in each experimental groups, was within 28.39mg/kg. And there were no significant metal concentration between control and experimental groups. Exceptionally, Cr and Ni level of control group was lower than experimental groups significantly. (p<0.05) and Cr and Ni level of experimental I group was lower than other experimental groups too. (p<0.05). But, Pb level of control group was higher than experimental groups significantly (p<0.05) Pb level of experimental I group was higher than other experimental groups(p<0.01) 2. In non-hazardous, hazardous and total metal concentration, there was no increase tendency in brain according to the high dose of OD(Ohjeoksan-Decoction) intake. Reversely, in experimental groups, hazardous metal concentration was decrease by high OD intake. (P<0.05) 3. Correlation among each metal in brain was various in each groups Briefly under the intake of Ohjeoksan-Decoction, that if very busy herb prescription , this study was defined within safety in brain metal level by P.O. during 10 days. But, there should be a more research about Pb increase by high dose OD intake
Kim, G.H.;Ryu, M.H.;Shin, Y.I.;Kim, H.I.;Kim, N.G.;Yang, Y.S.
Journal of Biomedical Engineering Research
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v.28
no.1
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pp.153-161
/
2007
Stroke is the second most significant disease leading to death in Korea. The conventional therapeutic approach is mainly based on physical training, however, it usually provides the limited degree of recovery of the normal brain function. The electric stimulation therapy is a novel and candidate approach with high potential for stroke recovery. The feasibility was validated by preliminary rat experiments in which the motor function was recovered up to 80% of the normal performance level. It is thought to improve the neural plasticity of the nerve tissues around the diseased area in the stroked brain. However, there are not so much research achievements in the electric stimulation for stroke recovery as for the Parkinson's disease or Epilepsy. This study aims at the developments of a wireless variable pulse generator using ZigBee communication for future implantation into human brain. ZigBee is widely used in wireless personal area network (WPAN) and home network applications due to its low power consumption and simplicity. The developed wireless pulse generator controlled by ZigBee can generate various electric stimulations without any distortion. The electric stimulation includes monophasic and biphasic pulse with the variation of shape parameters, which can affect the level of recovery. The developed system can be used for the telerehabilitation of stroke patient by remote control of brain stimulation via ZigBee and internet. Furthermore, the ZigBee connection used in this study provides the potential neural signal transmission method for the Brain-Machine Interface (BMI).
Using in vitro autoradiography with a digital autoradiography system and radioreceptor assay, the distribution and the binding characteristics of the muscarinic cholinergic receptors (mAChR) were studied in regions of rat brain. Radioreceptor assay revealed that mAChR could be measured with saturation binding assay in the brain and heart homogenates: No difference in Kd or Bmax of the brain or heart was found between the normal Wistar rats and SHR rats. Specific binding of $^3H$ quinuclidinyl benzilate (QNB) increased and saturation was reached by 2 hours after incubation with slide-mounted brain tissue. The distribution of mAChR was heterogeneous along the fields of brain. Affinity (Kd) of mAChR was not different significantly among cortex, hippocampus and caudate-putamen. No difference was found between normal rats and SHR strain. More receptors (Bmax) were found in the cortex and hippocampus than in the caudate-putamen in normal rats. More receptors were found in the cortex and caudate-putamen in SHR rats than in normal rats. Radioreceptor assay and digital autoradiographic analysis of affinity and number of mAChR gave the same results. With the above findings, we concluded that we could use digital autoradiographic system with $^3H$-QNB in the characterization of mAChR of rats and that the cortex and caudate-putamen of SHR strain rats have more receptors than those of normal rats.
The effects of dietary n-3 fatty acids, ${\alpha}$-linolenic acid (18:3), eicosapentaenoic acid (EPA, 20:5), and docosahexaenoic acid (DHA, 22:6), on brain phospholipid content and fatty acid composition were compared in rats fed with a diet containing constant ratios of saturated fatty acid/monounsaturated fatty acid/polyunsaturated fatty acid (PUFA) and n-3/n-6. The dietary fat in each diet was added at the level of 10%. In each diet, n-3 PUFA comprised two-thirds of the PUFA and the remaining one-third was linoleic acid (18:2). Dietary fat containing linoleic acid as the sole source of PUFA was also given to the control group. The content of brain phospholipid in the three n-3 PUFA groups was significantly lower than that of the linoleic acid group. This reduction was greater in the EPA and DHA groups than in the ${\alpha}$-linolenic acid group. The decrease in phospholipid content in rats fed n-3 fatty acid-rich diets was largely due to the decrease in the phosphatidylethanolamine fraction. Each dietary n-3 PUFA was found to affect the fatty acid composition of brain phospholipids; the most pronounced alteration was observed in phosphatidylethanolamine fraction. Furthermore, the proportion of DHA in the phosphatidylethanolamine fraction tended to be higher in the DHA group than in other PUFA groups. In conclusion, dietary ${\alpha}$-linolenic acid, EPA and DHA can influence the phospholipid content, phospholipid subclass, and fatty acid composition in rat brain.
Background: Heat stress orchestrates neurodegenerative disorders and results in the formation of reactive oxygen species that leads to cell death. Although the immunomodulatory effects of ginseng are well studied, the mechanism by which ginseng alleviates heat stress in the brain remains elusive. Methods: Rats were exposed to intermittent heat stress for 6 months, and brain samples were examined to elucidate survival and antiinflammatory effect after Korean Red Ginseng (KRG) treatment. Results: Intermittent long-term heat stress (ILTHS) upregulated the expression of cyclooxygenase 2 and inducible nitric oxide synthase, increasing infiltration of inflammatory cells (hematoxylin and eosin staining) and the level of proinflammatory cytokines [tumor necrosis factor α, interferon gamma (IFN-γ), interleukin (IL)-1β, IL-6], leading to cell death (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay) and elevated markers of oxidative stress damage (myeloperoxidase and malondialdehyde), resulting in the downregulation of antiapoptotic markers (Bcl-2 and Bcl-xL) and expression of estrogen receptor beta and brain-derived neurotrophic factor, key factors in regulating neuronal cell survival. In contrast, KRG mitigated ILTHS-induced release of proinflammatory mediators, upregulated the mRNA level of the antiinflammatory cytokine IL-10, and increased myeloperoxidase and malondialdehyde levels. In addition, KRG significantly decreased the expression of the proapoptotic marker (Bax), did not affect caspase-3 expression, but increased the expression of antiapoptotic markers (Bcl-2 and Bcl-xL). Furthermore, KRG significantly activated the expression of both estrogen receptor beta and brain-derived neurotrophic factor. Conclusion: ILTHS induced oxidative stress responses and inflammatory molecules, which can lead to impaired neurogenesis and ultimately neuronal death, whereas, KRG, being the antioxidant, inhibited neuronal damage and increased cell viability.
Chung, Suk-Jae;Ramanathan, Vikram;Brett, Claire M.;Giacomini, Kathleen M.
Journal of Pharmaceutical Investigation
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v.25
no.3
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pp.7-20
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1995
Taurine, a ${\beta}-amino$ acid, plays an important role as a neuromodulator and is necessary for the normal development of the brain. Since de novo synthesis of taurine in the brain is minimal and in vivo studies suggest that taurine dose not cross the blood-brain barrier, we examined whether the choroid plexus, the blood-cerebrospinal fluid (CSF) barrier, plays a role in taurine transport in the central nervous system. The uptake of $[^3H]-taurine$ into ATP depleted choroid plexus from rabbit was substantially greater in the presence of an inwardly directed $Na^+$ gradient taurine accumulation was negligible. A transient in side-negative potential gradient enhanced the $Na^+-driven$ uptake of taurine into the tissue slices, suggesting that the transport process is electrogenic, $Na^+-driven$ taurine uptake was saturable with an estimated $V_{max}$ of $111\;{\pm}\;20.2\;nmole/g/15\;min$ and a $K_M\;of\;99.8{\pm}29.9\;{\mu}M$. The estimated coupling ratio of $Na^+$ and taurine was $1.80\;{\pm}\;0.122.$$Na^+-dependent$ taurine uptake was significantly inhibited by ${\beta}-amino$ acids, but not by ${\alpha}-amino$ acids, indicating that the transporter is selective for ${\beta}-amino$ acids. Since it is known that the physiological concentration of taurine in the CSF is lower than that in the plasma, the active transport system we characterized may face the brush border (i.e., CSF facing) side of the choroid plexus and actively transport taurine out of the CSF. Therefore, we examined in vivo elimination of taurine from the CSF in the rat to determine whether elimination kinetics of taurine from the CSF is consistent with the in vitro study. Using a stereotaxic device, cannulaes were placed into the lateral ventricle and the cisterna magna of the rat. Radio-labelled taurine and inulin (a marker of CSF flow) were injected into the lateral ventricle, and the concentrations of the labelled compounds in the CSF were monitored for upto 3 hrs in the cisterna magna. The apparent clearance of taurine from CSF was greater than the estimated CSF flow (p<0.005) indicating that there is a clearance process in addition to the CSF flow. Taurine distribution into the choroid plexus was at least 10 fold higher than that found in other brain areas (e. g., cerebellum, olfactory bulb and cortex). When unlabelled taurine was co-administered with radio-labelled taurine, the apparent clearance of taurine was reduced (p<0.0l), suggesting a saturable disposition of taurine from CSF. Distribution of taurine into the choroid plexus, cerebellum, olfactory bulb and cortex was similarly diminished, indicating that the saturable uptake of taurine into these tissues is responsible for the non-linear disposition. A pharmacokinetic model involving first order elimination and saturable distribution described these data adequately. The Michaelis-Menten rate constant estimated from in vivo elimination study is similar to that obtained in the in vitro uptake experiment. Collectively, our results demonstrate that taurine is transported in the choroid plexus via a $Na^+-dependent,saturable$ and apparently ${\beta}-amino$ acid selective mechanism. This process may be functionally relevant to taurine homeostasis in the brain.
The concentration of neurotransmitters in rat brain was determined by HPLC-ECD (electrochemical detection) method and the effects of methanol extracts of some crude drugs, such as Polygala Radix, Myristicae Semen, Zizyphi Semen, Acori graminei Rhizoma, Visci Herba, Liriopsis Tuber, Myrrha on the concentration of neurotransmitters in the ethanol-treated rat brain were investigated. By the administration of ethanol, dopamine (DA), 3, 4-dihydroxyphenyl acetic acid (DOPAC) and serotonin (5-HT) levels in frontal cortex and 5-HT level in hippocampus were significantly increased compared with the neurotransmitter levels in the brain of saline-treated rats. The ${\gamma}$-aminobutyric acid (GABA) level in frontal cortex was decreased by the same treatment. There was a tendency that the DA level in frontal cortex and striatum of ethanol-treated rats were increased by the administration of crude drug extracts. Especially, Myrrha and Visci Herba significantly increased the DA level of frontal cortex in ethanol-treated rats, while they significantly decreased the 5-HT level in the same region of the brain. GABA level in striatum of ethanol-treated rats was significantly decreased by Myristicae Semen, Visci Herba and Myrrha. These results suggest that the tested crude drug extracts have selective interaction with neurotransmitters in specified region of central nervous system.
The purpose of this study was to evaluate histologically the effect of LiF-maleic acid added calcium aluminate(LM-CA) bone cement & CA-PMMA composite bone cement on the healing of calvarial defect in Sprague-Dawley rats. The critical size defects were surgically produced in the calvarial bone using the 8mm trephine bur. The rats were divided in three groups : In the control group, nothing was applied into the defect of each rat. LM-CA bone cement was implanted in the experimental group 1 and CA-PMMA composite bone cement was implanted in the experimental group 2. Rats were sacrificed at 2, 8 weeks after surgical procedure. The specimens were examined by histologic analysis, especially about the bone-cement interface and the response of surrounding tissue. The results are as follows; 1. In the control group, inflammatory infiltration was observed at 2 weeks. At 8 weeks, periosteum and duramater were continuously joined together in the defect area. But the center of defect area was filled up with the loose connective tissue. 2. In the experimental group 1, the bonding between implanted bone cement and the existing bone was seen, which more increased in 8 weeks than 2 weeks. Inflammatory infiltration and the dispersion of implanted bone cement particles were seen in both 2 weeks and 8 weeks. 3. In the experimental group 2, implanted bone itself had a dimensional stability and no bonding between implanted bone cement and the existing bone was seen in both 2 weeks and 8 weeks. Implanted bone cement was encapsulated by fibrous connective tissue. In addition, inflammatory infiltration was seen around implanted bone cement. On the basis of these results, when LM-CA bone cement or CA-PMMA composite bone cement was implanted in rat calvarial defect, LM-CA bone cement can be used as a bioactive bone graft material due to ability of bonding to the existing bone and CA-PMMA can be used as a graft material for augmentation of bone-volume due to dimensional stability.
$^{99m}Tc$ labeled PnAO(propylene amine oxime) derivatives have been widely studied as brain perfusion agents. We synthesized and characterized a PnAO derivative, (RR/SS/ meso)-4,8-diaza-3,9-dimethylundecane-2, 10-dione bisoxime(PRODD). Proton-NMR spectroscopy and thin layer chromatography(silica gel) were performed for its characterization. PRODD was labeled with $^{99m}Tc$ using stannous chloride as reducing agent. The labeling efficiency was determined to be about 85%. Brain uptakes of $4.16{\pm}0.42$ %ID/g and $3.24{\pm}0.13$ %ID/g were found after 10min and 30min after intravenous injection. Brain-to-blood ratios were 1.17 and 0.75 at 10 and 30 minutes, which were lower than 1.3 and 1.9 of the ratios with commercial ${\pm}$-HMPAO. Autoradiographs of rat brain sections showed the gray matter to white matter ratios of $1.13{\pm}0.10$ at 30 min after intravenous injection, which was lower than $1.94{\pm}0.19$ of commercial $^{99m}Tc$-HMPAO. With the above findings, we concluded that the lipophilic $^{99m}Tc$-PRODD complex was able to cross the blood-brain barrier, however the complex showed lower uptake than $^{99m}Tc$-HMPAO in mouse or rat brains. We could suggest possibility that PRODD could be used as another $^{99m}Tc$ chelator.
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