• The Korean Journal of Physiology and Pharmacology
• /
• 제2권4호
• /
• pp.511-519
• /
• 1998

This study investigated the role of nitric oxide on the oxidative damage in gastric mucosa of rats which received ischemia/reperfusion and its relation to mucus. Nitric oxide synthesis modulators such as L-arginine and $N^G-nitro-L-arginine$ methyl ester, and sodium nitroprusside, a nitric oxide donor, were injected intraperitoneally to the rats 30 min prior to ischemia/reperfusion which was induced by clamping the celiac artery and the superior mesenteric artery for 30 min and reperfusion for 1 h. Lipid peroxide production, the contents of glutathione and mucus, and glutathione peroxidase activities of gastric mucosa were determined. Histological observation of gastric mucosa was performed by using hematoxylin-eosin staining and scanning electron microscopy. The result showed that ischemia/reperfusion increased lipid peroxide production and decreased the contents of glutathione and mucus as well as glutathione peroxidase activities of gastric mucosa. Ischemia/reperfusion induced gastric erosion and gross epithelial disruption of gastric mucosa. Pretreatment of L-arginine, a substrate for nitric oxide synthase, and sodium nitroprusside prevented ischemia/reperfusion-induced alterations of gastric mucosa. However, $N^G-nitro-$ L- arginine methyl ester, a nitric oxide synthase inhibitor, deteriorated oxidative damage induced by ischemia/reperfusion. In conclusion, nitric oxide has an antioxidant defensive role on gastric mucosa by maintaining mucus, glutathione, and glutathione peroxidase of gastric mucosa.

• Archives of Pharmacal Research
• /
• 제22권5호
• /
• pp.479-484
• /
• 1999

In this study, the effects of ursodeoxycholic acid (UDCA) on ischemia/reperfusion injury were investigated on isolated heart perfusion model. Hearts were perfused with oxygenated Krebs-Henseleit solution (pH 7.4, $37^{\circ}C$) on a Langendroff apparatus. After equilibration, isolated hearts were treated with UDCA 20 to 160 $\mu$M or vehicle (0.04% DMSO) for 10 min before the onset of ischemia. After global ischemia (30 min), ischemic hearts were reperfused and allowed to recover for 30 min. The physiological (i.e. heart rate, left ventricular developed pressure, coronary flow, double product and time to contracture formation) and biochemical (lactate dehydrogenase; LDH) parameters were evaluated. In vehicle-treated group, time to contracture formation was 21.4 min during ischemia, LVDP was 18.5 mmHg at the endpoint or reperfusion and LDH activity in total reperfusion effluent was 54.0 U/L. Cardioprotective effects of UDCA against ischemia/reperfusion consisted of a reduced TTC $(EC_{25}=97.3{\mu}M)$, reduced LDH release and enhanced recovery of cardiac contractile function during reperfusion. Especially, the treatments of UDCA 80 and $160 {\mu}M $ significantly increased LVDP and reduced LDH release. Our findings suggest that UDCA ameliorates ischemia/reperfusion-induced myocardial damage.

• 대한수의학회지
• /
• 제37권1호
• /
• pp.111-117
• /
• 1997

This study was carried out determine the effect of renal ischemia on amino acid transport in rabbit renal cortical slices. The animal models of renal ischemia induced experimentally by clamping the renal artery. These results were summarized as follows: 1. The uptake of amino acids lysine and ${\alpha}$-aminobutyrate(AIB), dicarboxylate succinate and organic anion PAH in cortical slices was normal or increased after 30 or 60 min of ischemia in vivo. 2. In a 30 min ischemic kidney, the slice uptake of amino acids was returned to the control level by 30 min of reflow. In a 60 or 90 min ischemic kidney, the lysine uptake was returned to the control level after of reflow, but the uptake of AIB and succinate was significantly reduced during reflow period of 30-120 min. 3. Oxygen consumption in cortical slices was increased after 30 min of ischemia but was not altered by 60 min of ischemia. This results indicat that transient ischemia caused increasing of amino acid uptake in renal cortical slices without metabolic disorder of renal proximal tubule.

• 대한한의학회지
• /
• 제39권4호
• /
• pp.1-15
• /
• 2018

Objectives: Cerebral ischemia results from a variety of causes that cerebral blood flow is reduced due to a transient or permanent occlusion of cerebral arteries. Reactive astrocytes and microglial activation plays an important role in the neuronal cell death during ischemic insult. Acupunctural treatment is effective for symptom improvement in cerebrovascular accident, including cerebral ischemia. Methods: In the present study, the effects of acupuncture at the ST40 acupoint on short-term memory and apoptosis in the hippocampal CA1 region following transient global cerebral ischemia were investigated using gerbils. Transient global ischemia was induced by occlusion of both common carotid arteries with aneurysm clips for 5 min. Acupuncture stimulation was conducted once daily for 7 consecutive days, starting one day after surgery. Results: In the present results, ischemia induction deteriorated short term memory, increased apoptosis, and induced reactive astrocyte and microglial activation. Acupuncture at ST40 acupoint ameliorated ischemia-induced short-term memory impairment by suppressing apoptosis in the hippocampus through down-regulation of reactive astrocytes and microglial activation. Conclusion: The present study suggests that acupuncture at the ST40 acupoint can be used for treatment of patients with cerebral stroke.

• 대한한의학회지
• /
• 제30권2호
• /
• pp.1-16
• /
• 2009

Objectives: This study investigated the effect of Yukmijihwangtang on cerebral ischemia-induced learning and memory impairment by middle cerebral artery (MCA) occlusion in rats. Methods: The ability of learning and memory of rats was measured using the eight-arm radial maze and the passive avoidance test, and profile of cholinergic neuron was assessed in the medial septum and hippocampus region by immuno-histochemistry. Results: 1. No differences were found between groups in the number of correct choices in acquisition performance during the eight-arm radial maze task. 2. No differences were found between groups on day 1 in the error rate in acquisition performance, which is defined as the number of enters into the same arm more than once within five minutes. After 5 to 6 days of test, the number of errors was significantly reduced in the Yukmijihwangtang group (forebrain ischemia group with Yukmijihwangtang treatment), compared with the ischemia group. 3. The memory processes significantly improved in the Yukmijihwangtang group according to results of the passive avoidance test. 4. The appearance of AchE (acetylcholinesterase) in the CA1 region of hippocampus significantly decreased in the ischemia group, compared with the sham group (untreated group). The appearance of AchE in the same region significantly increased in the Yukmijihwangtang group, compared with the ischemia group. 5. The appearance of ChAT (choline acetyltransferase) in the CA1 region of the hippocampus and medial septum decreased in the ischemia group, compared with the sham group. The appearance of ChAT in the same region significantly increased in the Yukmijihwangtang group, compared with the ischemia group Conclusions: This study provides evidence that Yukmijihwangtang is effective for reviving the ability of learning and memory and damaged neurons in rats with experimental cerebral ischemia.

• 대한한의학회지
• /
• 제26권3호
• /
• pp.146-161
• /
• 2005

Objectives : This study investigated neuroprotective effects of Polygoni Multiflori Radix on cerebral ischemia of hyperlipidemic rats. Methods : Effects of Polygoni Multiflori Radix were evaluated with changes of infarct size after He focal cerebral ischemia induced by the middle cerebral artery occlusion, changes of pyramidal neurons and expressions of Bax and Bcl-2 apoptosis regulating factors after global cerebral ischemia, and changes of serum lipid revels after cerebral ischemia. Results & Conclusions : Results obtained were as follows; 1. Polygoni Multiflori Radix did net reduce the focal cerebral infarct size induced by the middle cerebral artery occlusion under both hyperlipidemic and normal-lipid conditions. 2. Polygoni Multiflori Radix significantly reduced the increase of neuronal cell death in CAl region of hippocampus induced by the global cerebral ischemia under both hyperlipidemic and normal-lipid conditions. 3. Polygoni Multiflori Radix significantly reduced the increase of Bax expression in the CAl region of the hippocampus induced by global cerebral ischemia under both hyperlipidemic and normal-lipid conditions. 4. Polygoni Multiflori Radix significantly increased Bc1-2 expression in the CA1 region of the hippocampus after global cerebral ischemia under normal-lipid condition, but was not effective on that under hyperlipidemic condition. 5. Polygoni Multiflori Radix was not effective on serum total-cholesterol, HDL-cholesterol, LDL-cholesterol and triglyceride levels under normal-lipid conditions, irrespective of focal cerebral infarct or global cerebral ischemia. 6. Polygoni Multiflori Radix significantly reduced the increase of serum total-cholesterol and triglyceride levels, and increased serum LDL-cholesterol level under hyperlipidemic conditions, irrespective of foc31 cerebral infarct or global cerebral ischemia.

• Journal of Korean Neurosurgical Society
• /
• 제54권1호
• /
• pp.1-7
• /
• 2013

Objective : This study was undertaken in the belief that the atypical antipsychotic drug quetiapine could prevent apoptosis in the penumbra region following ischemia, taking into account findings that show 5-hydroxytryptamine-2 receptor blockers can prevent apoptosis. Methods : We created 5 groups, each containing 6 animals. Nothing was done on the K-I group used for comparisons with the other groups to make sure adequate ischemia had been achieved. The K-II group was sacrificed on the 1st day after transient focal cerebral ischemia and the K-III group on the 3rd day. The D-I group was administered quetiapine following ischemia and sacrificed on the 1st day while the D-II group was administered quetiapine every day following the ischemia and sacrificed on the 3rd day. The samples were stained with the immunochemical TUNEL method and the number of apoptotic cells were counted. Results : There was a significant difference between the first and third day control groups (K-II/K-III : p=0.004) and this indicates that apoptotic cell death increases with time. This increase was not encountered in the drug groups (D-I/D-II : p=1.00). Statistical analysis of immunohistochemical data revealed that quetiapine decreased the apoptotic cell death that normally increased with time. Conclusion : Quetiapine is already in clinical use and is a safe drug, in contrast to many substances that are used to prevent ischemia and are not normally used clinically. Our results and the literature data indicate that quetiapine could help both as a neuronal protector and to resolve neuropsychiatric problems caused by the ischemia in cerebral ischemia cases.

• 대한한방내과학회지
• /
• 제20권1호
• /
• pp.111-121
• /
• 1999

Cervus elaphus (CE), being known to reinforce Kidney, have tested to study the effects concerning damages of renal tissue induced by oxygen free radicals. I had observed the effects of CE extract on damages of rat's kidney following ischemia and reflow. Before ischemia was caused, CE extract was applied $0.2m{\ell}$ per 250g through femoral vein in ischemia and reflow group and normal sailine was applied in normal group, Ischemia was caused by renal artery's clamp for 60 min and reflowed by clamp remove after 30 min. It was increased on the content of lipid peroxidation, activies and type conversion ratio of xanthine oxidase following ischemia and reflow. by clamp remove after 30 min. It was increased on the content of lipid peroxidation, activies and type conversion ratio of xanthine oxidase following ischemia and reflow. However, they were decreased when CE extract was pre-applied. Glutathione level was decreased in ischemia and reflow group, and increased in CE extract's pre-applied group. However, it could not seen special changes on aldehyde oxidase activities, either. In conclusion, CE extract recovers the damage of kidney due to ischemia and reflow by decreasing the lipid peroxidation.

• 한방재활의학과학회지
• /
• 제21권2호
• /
• pp.15-30
• /
• 2011

Objectives : The present study investigated the effects of Achyranthis Radix on short-term memory, apoptotic neuronal cell death in the hippocampus following transient global ischemia in gerbils. Methods : The gerbils were divided into 5 groups(n=10); Sham operation group, ischemia-induced group, ischemia-induced and 50 mg/kg Achyranthis Radix-treated group, ischemia-induced and 100 mg/kg Achyranthis Radix-treated group, ischemia-induced and 200 mg/kg Achyranthis Radix-treated group. For this study, a step-down avoidance task, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL) assay, immunohistochemistry for caspase-3 and BrdU(5-Bromo-2'-deoxyuridine), and western blotting for bax, bcl-2 were performed. Results : The results revealed that ischemic injury impaired short-term memory and increased apoototic neuronal cell death in the hippocampal CA1(cornu ammonis area 1) region. Ischemic injury enhanced cell proliferation in the hippocampal CA1 region, the compensatory and adaptive process for excessive apoptosis. Achyranthis Radix treatment improved short-term memory by suppressing ischemia-induced apoptotic neuronal cell death in the hippocampal CA1 region. Also, Achyranthis Radix suppressed the ischemia-induced increase in cell proliferation in the hippocampal CA1 region. Conclusions : We showed that Achyranthis Radix alleviates ischemia-induced apoptotic neuronal cell death, thus facilitates the recovery of short-term memory impairment induced by ischemic cerebral injury.

• Molecules and Cells
• /
• 제19권3호
• /
• pp.382-390
• /
• 2005

Calcium-binding proteins are thought to play important roles in calcium buffering. The present study investigated the effects of ischemia and reperfusion on calbindin D28K, calretinin, and parvalbumin immunoreactivity in the ganglion cell layer of the rabbit. Rabbits were administered ischemic damage by increasing the intraocular pressure. After 60 and 90 min of ischemia, reperfusion (7 d) was allowed to occur. The b-wave of the electroretinogram (ERG) was reduced by more than 50% and almost 80% in retina given ischemia for 60 and 90 min, respectively. The oscillatory potential (OPs) wave was reduced approximately 50% at 60 min ischemia and 70% at 90 min ischemia. In both normal and ischemic-treated retina, calcium-binding protein immunoreactivity was seen in many cells in the ganglion cell layer. In eyes subjected to 60 min ischemia, there was a decrease of the density of calbindin D28K- (8.29%), calretinin- (14.44%), and parvalbumin- (26.83%) immunoreactive (IR) cells compared to the control retina. In eyes subjected to 90 min ischemia, there was a higher decrease of the density of calbindin D28K- (18.48%), calretinin- (33.59%), and parvalbumin- (54.26%) IR cells than at 60 min. Some calcium-binding protein-IR neurons, especially calretinin-IR neurons, showed aggregations that were abnormally packed together in retina subjected to ischemia for 90 min. The results show that calbindin D28K-, calretinin-, and parvalbumin-IR cells in the ganglion cell layer are susceptible to ischemic damage and reperfusion. The degree of reduction varied among different calcium-binding proteins and ischemic damage times. These results suggest that calbindin D28K-containing neurons are less susceptible to ischemic damage than calretinin- and parvalbumin-containing neurons in the ganglion cell layer of rabbit retina.