Alterations of H-and M-isozymes of Lactic Dehydrogenase(LDH) were observed in the various tissues after exposing the rats to 50ppm and 250ppm of sulfur dioxide. These isozymes of the respective tissue were separated by Diethlaminoethyl (DTAE)-cellulose from the tissue homogenates of brain, lung and muscle, presenting the activities by rate of reduction of nicotinamide-adenine-dinucleotide ($NAD^+$). Pure LDH and the coenzyme ($NAD^+$) were directly treated with sulfur dioxide in vitro in order to find out the direct to sulfur dioxide on LDH and $NAD^+$ and the results were as follows. 1. In the normal tissues, the H-isozyme activity was dominant in the brain and heart, and the M-isozyme in the muscle. 2. In the lung tissue of normal rats, there was no difference between the activity of H-and M-type of LDH. 3. When rats inhale sulfur dioxide gas in concentration of 50ppm and 250ppm, it appeared that the H-type tend to be suppressed in aerobic tissues and the M-type in anaerobic tissues. 4. In the lung tissue exposed to sulfur dioxide, both the LDH activities were suppressed. 5. It seems that LDH and the coenzyme ($NAD^+$) are not directly affected by exposing in sulfur dioxide gas.
Some effects of dietary conditions on the metabolism of nucleic acid and protein in organs of the Albino Rats have been studied. The young rats to be examined were fed on the control diet and the diets deprived of one component among protein, carbohydrate, and lipid, such as protein free diet (PF: 432 kcal/100g) carbohydrate free diet (CF: 432kcal/100g), and lipid free diet (LF: 392kcal/100g) for three, seven, and fifteen days, respectively. The contents of DNA and RNA in the liver and the brain, and also those of protein-nitrogen(PN) and nonprotein-nitrogen (NPN) in the live, the brain, and the serum have been measured. The results are as followe: 1. The contents of DNA per gram of liver were increased by feeding on protein free diet. It is concluded that the critical factor for the result is not the increase in the rates of DNA syntheses, but the decrease in the turnover rates of DNA. 2. The metabolism of DNA in the liver showed the normal status by feeding on carbohydrate free diet. On the other hand, the rates of DNA syntheses were increased by feeding on lipid free diet. 3. The rates of DNA syntheses in the brain were decreased by feeding on the unbalanced diet, such as protein free, carbohydrete free, and lipid free diet. 4. In the liver and the brain, the rates of DNA syntheses were decreased by feeding on protein free diet. But the rates showed the normal status by feeding on the carbohydrate free diet, and also showed the similar metabolism to that in the case of the control group by feeding on lipid free diet. 5. In the liver, the rates of protein syntheses were decreased, whereas the contents of nonprotein-nitrogen were increased by feeding on protein free diet. 6. In the liver and the brain, the protein syntheses showed the more increasing rates than the rates in the case of the control diet by feeding on lipid free diet. 7. In the serum, the contents of protein did not change in a short period, also the insufficient feeling on protein was examined. It is clear that in the liver the rates of protein syntheses are decreased and the rates of protein catabolism are increased, since the rates of nucleic acid syntheses are decreased by feeding on the protein free diet. On the other hand, it is considered that in the brain the turnover rates of protein does not have correlation with the rates of nucleic acid syntheses, also these are decreased by feeding on protein free diet. And also it is believed that the phenomena of homeostasis for carrying the normal metabolism of nucleic acid and protein in the liver and the brain are operated in a short period as possible, by feeding on carbohydrate free and lipid free diets.
Kyungisan (KGS) has been used in oriental medicine for many centuries as a therapeutic agent for treatment of stroke caused by deficiency of qi(氣虛). This study was performed to evaluate effects of KGS extract on the regional cerebral blood flow(rCBF) and mean arterial blood pressure(MABP) in rats. The result of this study were as follow ; 1. KGS significantly increased rCBF irrelevant to MABP in normal rats, 2. To prescribe KGS after pretreatment with indomethacin(IDN) decreased rCBF as compared with control group to administered only KGS in normal rats. But the change of MABP is not significantly as compared with control group. 3. To prescribe KGS after pretreatment with methylen blue( MTB) decreased MABP and rCBF as compared with control group to administered only KGS in normal rats. Especially, it significantly decreased rCBF. These results suggest that KGS increase rCBF by enlargement diameter of pial artery in brain. The active mechanism of KGS is related with prostaglandin activated by cyclooxygenase. So, I suggest that KGS has an anti-ischemic effect through the improvement of cerebral blood flow and can be used for stroke.
The aim of this study was to evaluate the involvement of CPP32 (caspase-3), one of the death-related enzymes, in the course of experimental autoimmune encephalomyelitis (EAE). EAE was induced in Lewis rats immunized with an emulsion of rat spinal cord homogenate with complete Freunds adjuvant supplemented with Mycobacterium tuberculosis (H37Ra, 5mg/ml). The expression of CPP32 in the spinal cords of rats with EAE was studied. In normal rat spinal cords, CPP32 is constitutively, but weakly, expressed in neurons and some neuroglial cells. In the EAE spinal cords, many inflammatory cells were positive for CPP 32, and the majority of CPP32(+) cells were identified as ED1(+) macrophages. During this stage of EAE, the number of CPP32(+) cells in brain cells, including neurons and astrocytes, increased, and these cells also had increased CPP32 immunoreactivity. CPP32 immunor eactivity was not always matched with apoptosis of inflammatory cells in EAE lesions. We speculate that CPP32, which is constitutlvely expressed in brain cells, increases in response to neuroimmunological stimulation in both brain neuronal cells and inflammatory cells. The functional role of CPP32 in neuroimmunological disorders is discussed.
Lee, Jae Hoon;Kam, Eun Hee;Kim, Jeong Min;Kim, So Yeon;Kim, Eun Jeong;Cheon, So Yeong;Koo, Bon-Nyeo
Biomolecules & Therapeutics
/
v.25
no.2
/
pp.149-157
/
2017
The interleukin-1 receptor antagonist (IL-1RA) is a potential stroke treatment candidate. Intranasal delivery is a novel method thereby a therapeutic protein can be penetrated into the brain parenchyma by bypassing the blood-brain barrier. Thus, this study tested whether intranasal IL-1RA can provide neuroprotection and brain penetration in transient cerebral ischemia. In male Sprague-Dawley rats, focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) for 1 h. The rats simultaneously received 50 mg/kg human IL-1RA through the intranasal (IN group) or intraperitoneal route (IP group). The other rats were given 0.5 mL/kg normal saline (EC group). Neurobehavioral function, infarct size, and the concentration of the administered human IL-1RA in the brain tissue were assessed. In addition, the cellular distribution of intranasal IL-1RA in the brain and its effect on proinflammatory cytokines expression were evaluated. Intranasal IL-1RA improved neurological deficit and reduced infarct size until 7 days after MCAO (p<0.05). The concentrations of the human IL-1RA in the brain tissue 24 h after MCAO were significantly greater in the IN group than in the IP group (p<0.05). The human IL-1RA was confirmed to be co-localized with neuron and microglia. Furthermore, the IN group had lower expression of $interleukin-1{\beta}$ and tumor necrosis $factor-{\alpha}$ at 6 h after MCAO than the EC group (p<0.05). These results suggest that intranasal IL-1RA can reach the brain parenchyma more efficiently and provide superior neuroprotection in the transient focal cerebral ischemia.
Montilla, Pedro;Barcos, Montserrat;Munoz, Maria C.;Bujalance, Inmaculada;Munoz-Castaneda, Juan R.;Tunez, Isaac
BMB Reports
/
v.38
no.5
/
pp.539-544
/
2005
We have studied the effects of red wine on brain oxidative stress and nephropathy in streptozotocin (STZ)-induced diabetic rats. Diabetes was induced in Wistar rats with a single intraperitonally injection of STZ (50 mg/kg). Two weeks before and four weeks after injection, red wine was given orally in both normal and diabetic rats. Blood samples were taken from the neck vascular trunk in order to determine the glucose, triglycerides, total cholesterol, HDL-cholesterol (HDL-c), atherogenic index (AI), total protein, blood urea nitrogen (BUN), creatinine, insulin, lipid peroxidation products, reduced glutathione (GSH) and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities. As well, we estimated the lipid peroxidtion, GSH and SOD, GSH-Px and catalase activities in brain and renal homogenates, and the excretion of albumin, proteins and glucose in urine over 24 h period. The administration of STZ caused significant increases in levels of glycosuria, proteinuria, albuminuria, glycemia, total cholesterol and AI, as well as in lipid peroxidation products in the brain, plasma and kidney, whereas it decreased the GSH content and SOD, GSH-Px and catalase activities. Treatment with red wine significantly prevented the changes induced by STZ. These data suggested that red wine has a protective effect against brain oxidative stress, diabetic nephropathy and diabetes induced by STZ, as well as it protects against hypercholesterolemia and atherogenic risk.
The aim of this study was to observe whether the dietary supplementation of docosahexaenoic acid(DHA). In growing rats requires extra supplementation of arachidonic acid(AA) for brain development. Sprague-Dawley rats were divided into three groups, each fed a different diet. In the FO group, dams were fed a DHA-rich FO diet during pregnancy and lactation and pups were fed the same diet until 10 weeks old. In the AO group dams and pups were similarly fed a FO diet after weaning. DHA and AA were most effetively deposited in the developing brain during pregnancy and lactation in rats. However, FO-W pups showed significantly lower level of DHA at 0-3 weeks compared with the FO and AO groups and than slowly increased DHA levels to about 87% of other groups at 10 weeks with the introduction of the FO diet after weaning. The total amount of DNA in whole brain rapidly reached a maximum level at 3 weeks and then was sustained at a constant level after 5 weeks of age. The DNA content was positively correlated with DHA level but not with AA level in the developing brain. DNA content was significantly lower in the FO-W group compared to the FO and AO group at 3 weeks of age. However, the DNA content of brain in FO-W pups increased to 80% of the FO group level at 10 weeks after feeding the FO diet after weaning. The relative percentage of AA in brain lipids was significantly reduced in the early stage of brain development when only DHA was supplemented. However, DHA supplementation had no significant effect on the incorporation of AA when the approximately 35% of LA in the FO diet was substituted by preformed AA. These results suggest that large quantities of DHA could interfere with the normal conversion of LA to AA if LA is not supplemented enough together with DHA. Therefore, high DHA supplementation may require preformed AA in the diet even though AA has no significant correlation with the DNA content in brain. DHA supplementation after weaning also improved the incorporation of DHA into brain and content of DNA even though brain development was almost completed, suggesting that a low level of DHA supplementation without AA addition might be necessary to improve brain development during infancy as well as during pregnancy and lactation.
Objective : The study was done to investigate Scrophularia buergeriana Miquel's effects in the genomic level, by measuring gene expression in hyperthyroid induced rats using cDNA micro array. Methods : Spargue-Dawley rats were separated into three groups(each with 10 rats). Except normal group, the other two groups were treated with Sodium levothyroxine $160{\mu}g$/kg/days for 5 days by oral administration. After 2 hours of the last intake of Sodium levothyroxine on two experimental group, one group was treated Scrophularia buergeriana Miquel extract 1.0g/kg/days for 3 days. The other groups(normal group, administration group) was treated normal saline 1.0g/kg/days for 3 days. Gene expression of hyperthyroid rats were measured after medication of solid extract of Scrophularia buergeriana Miquel with cDNA microarray. Results : In thyroid tissue, the numbers of the genes showed over twice increase and decrease in the control group compared to the normal group were 296, in the Scrophularia buergeriana Miquel administration group compared to the normal group were 859 and in the hypothalamus, the numbers of the genes showed over twice increase and decrease in the control group compared to the normal group were 416, in the Scrophularia buergeriana Miquel administration group compared to the normal group were 391. Conclusion : According to the above results, it is suggested that Scrophulari buergeriana Miquel suppress hyperthyroidism effectively and regulate the gene expression in the thyroid and brain.
Sun, Jing He;Joh, Chul W;Ahn, Young Hwan;Park, Chan Hee;Shim, Chull;Park, Kyung Bae;Cho, Kyung Gi
Journal of Korean Neurosurgical Society
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v.29
no.10
/
pp.1309-1315
/
2000
Objectives : We performed an in vivo experiment to investigate the effect of $^{166}Holmium$ and $^{166}Holmium$-chitosan complex($^{166}Ho$-CHICO) on the normal brain of rats and to determine the sublethal dose of $^{166}Ho$-CHICO. Materials and Methods : $^{166}Ho$ is a beta and gamma ray emitter. $^{166}Ho$-CHICO is a novel radio-pharmaceutical complex with chitosan to facilitate the transport of $^{166}Ho$ obtained from Korea Atomic Energy Research Center(Taejon, Korea). It is in acidic form and becomes gel state at alkaline pH. One hundred and seventy consecutive rats were divided into four groups : $^{166}Ho$ treated(n=50), $^{166}Ho$-CHICO treated(n=57), saline treated(n=5) and chitosan treated(n=5) groups. $^{166}Ho$ and $^{166}Ho$-CHICO were injected into the rat brain stereotactically with various doses of 0.1mCi/$20{\mu}l$, 0.2mCi/$20{\mu}l$, 0.3mCi/$20{\mu}l$, and 0.4mCi/$20{\mu}l$ using an automated microinjector. Nuclear imaging, histopathological and hematological studies were performed in 10 rats in each group at 1 day, 3days, 7 days, 1 month and 3 months after the injections. Results : An infiltration of inflammatory cells and necrotic changes were noted in $^{166}Ho$ treated group at 1 week after the injection. A wedge-shaped tissue defect due to necrosis, lined with infiltrated glial cells in $^{166}Ho$ treated group and a cystic defect lined with reactive astroglial cells in $^{166}Holmium$-CHICO treated group at 3 months after the injection were observed. $^{166}Ho$ alone without chitosan leaked out and caused necrotic lesion on the cerebral surface but $^{166}Holmium$-CHICO treated group did not show this feature. As the dose of $^{166}Ho$ increased, the mortality rates were also increased. The mortality rate of the $^{166}Holmium$-CHICO group was higher than the $^{166}Ho$ treated group at a dose of 0.4mCi/$20{\mu}l$/300g. There was no detectable radioactivity due to the leakage or extravasation from the injected site of the brain on the scintigraphy performed at 1 hour, 24 hours and 48 hours after the injection. There was also no detectable activity of $^{166}Holmium$-CHICO in other organs including spleen, liver and kidney. Conclusions : $^{166}Ho$-CHICO did not leak out to the critical cortical surface of the brain from the injection site and induced radiation changes of the parenchyma around the injection site without cortical damage. The sublethal dose of $^{166}Ho$-CHICO for the normal brain in rats was determined to be 0.2mCi/$20{\mu}l$/300g.
Proceedings of the Korean Society for Emotion and Sensibility Conference
/
2009.11a
/
pp.183-185
/
2009
As imaging technology develops, magnetic resonance imaging (MRI) techniques have contributed to the understanding of brain function by providing anatomical structure of the brain and functional imaging related to information processing. Manganese-enhanced MRI (MEMRI) techniques can provide useful information about functions of the nervous system. However, systematic studies regarding information processing of pain have not been conducted. The purpose of this study was to detect brain activation during painful electrical stimulation using MEMRI with high spatial resolution. Male Sprague-Dawley rats (250-300 g) were divided into 3 groups: normal control, sham stimulation, and electric stimulation. Rats were anesthetized with 2.5% isoflurane for surgery. Polyethylene catheter (PE-10) was placed in the external carotid artery to administrate mannitol and MnCl2. The blood brain barrier (BBB) was broken by 20% D-mannitol under anesthesia mixed with urethane and a-chloralose. The hind limb was electrically stimulated with a 2Hz (10V) frequency while MnCl2 was infused. Brain activation induced by electrical stimulation was detected using a 4.7 T MRI. Remarkable signal enhancement was observed in the primary sensory that corresponds to sensory tactile stimulation at the hind limb region. These results suggest that signal enhancement is related to functional activation following electrical stimulation of the peripheral receptive field.
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