• The Korean Journal of Pharmacology
• /
• v.26 no.1
• /
• pp.7-12
• /
• 1990

Cyclobuxine D is a steroidal alkaloid, which was extracted from Buxus microphylla var. koreana Nakai. In our previous studies, we clarified several pharmacological actions of cyclobuxine D: an antiinflammatory action, hypotensive and bradycardiac effects, negative inotropic effects on the several smooth muscles and cardiac muscle. The present study was undertaken to elucidate possible mechanisms by protection of myocardial tells from ischemia and reperfusion induced derangement in cardiac function and metabolism by cyclobuxine D. For this purpose, the isolated rat heart was used. Rat hearts were perfused for 60 min under ischemia conditions in the presence and absence of cyclobuxine D and verapamil, and for 30 min under reperfusion conditions. Ischemia produced a marked decline in contractile force, an increase of resting tension, an immediate release of ATP metabolites and an accumulation of calcium in the left ventricle. Cyclobuxine D (100ng/ml) ameliorated the myocardial injury produced by ischemia.

• Korean Journal of Acupuncture
• /
• v.22 no.4
• /
• pp.43-56
• /
• 2005

Objectives : The acupuncture has been used as treatment of disease in the oriental medicine. In this study, it was investigated at had an effects of Heart JEONGGYEOK(心正格) of SAAM five evolutive phase acupuncture techniques(舍岩五行鑛法) for appling deficiency in the heart induced by experimental focal ischemia. Materials and methods : The focal ischemia was induced by middle cerebral artery occlusion for 2hours. The groups divided into 6 groups, normal(intactness group), control(no therapy group after ischemia-induced), AT1(reinforcing acupoint of Heart JEONGGYEOK : acupuncture therapy group at LR1, HT9 after ischemia-induced), AT2(reinforcing acupoint of Kidney JEONGGYEOK : acupuncture therapy group at LU8, KI7 after ischemia-induced) AT3(combination of reinforcing acupoint of Heart JEONGGYEOK and Kidney JEONGGYEOK : acupuncture therapy group at LR1, HT9, LU8, KI7 after ischemia-induced) AT4(reinforcing and reducing acupoint of Heart JEONGGYEOK : acupuncture therapy group at LR1, HT9, HT3, KI10 after ischemia-induced), AT4(reinforcing and reducing acupoint of Heart JEONGGYEOK : acupuncture therapy group at LRI, HT9, HT3, KI10 after ischemia-induced). Acupuncture therapy was carried out during 3 weeks after focal ischemia-induced. Eight-arm radial maze was used for the behavioral task and neuropretective effect of acupuncture therapy was observed by Cresyl violet, AchE, ChAT-stain. Results : The error rate in the eight-arm radial maze task was significantly decreased in AT3 group on 3days, in AT1 and AT4 groups on 4days, in AT3 and AT4 groups on 5days compared to the control group. The rate of correct choice was significantly increased AT4 group compared to the control group. The density of neurons in the hippocampal CA1 were significantly increased in all experiment groups, AT1, AT2, AT3 and AT4 groups compared to the control group. The density of AchE in the hippocampal CA1 was significantly increased in AT4 group compared to the control group. The density of ChAT in the hippocampal CA1 were significantly increased in AT1 and AT3 group compared to the control group. Conclusions : These results suggest that reinforcing and reducing acupoint of Heart JEONGGYEOK could be used as a medication for controlling the stroke by deficiency in the heart.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.22 no.6
• /
• pp.1487-1494
• /
• 2008

This study was conducted to determine the effect of Gagamjeongji-hwan (JJH)(Jiajiandingzhi-wan) and Evoidae Fructus (EF) on learning and memory disturbance and neuronal damage induced by focal ischemia in the rat. Rats were used for testing in the following three. Morris Water Maze, Cholineacetyltransferase (ChAT) immunohistochemistry, acetylcholine esterase (AchE) histochemistry. JJH+ISCH group (ischemia-induced rats pretreated with JJH) and EF+ISCH group (ischemia-induced rats pretreated with EF) significantly reduced the latency of swimming time, compared with those of ISCH group (ischemia-induced rats) in morris water maze acquisition test. JJH+ISCH group attenuated ischemia.induced learning and memory damage in morris water maze retention test. The density of ChAT neurons of the JJH+ISCH and EF+ISCH group in the hippocampal CA1 area was increased, compared to that of SAL+ISCH group (ischemia-induced rats pretreated with SAL). The density of AchE neurons of the JJH+ISCH and EF+ISCH group in the hippocampal CA1 and CA3 area was increased, compared to that of SAL+ISCH group. These results suggest that Gagamjeongji-hwan (JJH) and Evodiae Fructus (EF) may have significant protective effects on ischemia-induced brain damage and memory impairments.

• The Korean Journal of Physiology and Pharmacology
• /
• v.1 no.6
• /
• pp.673-679
• /
• 1997

It has been generally accepted that glutamate mediates the ischemic brain damage, excitotoxicity, and induces release of neurotransmitters, including norepinephrine(NE), in ischemic milieu. In the present study, the role of nitric oxide(NO) in the ischemia-induced $[^3H]norepinephrine([^3H]NE)$ release from cortex slices of the rat was examined. Ischemia, deprivation of oxygen and glucose from $Mg^{2+}-free$ artificial cerebrospinal fluid, induced significant release of $[^3H]NE$ from cortex slices. This ischemia-induced $[^3H]NE$ release was significantly attenuated by glutamatergic neurotransmission modifiers. $N^G-nitro-L-arginine$ methyl ester(L-NAME), $N^G-monomethyl-L-arginine$ (L-NMMA) or 7-nitroindazole, nitric oxide synthase inhibitors attenuated the ischemia-evoked $[^3H]NE$ release. Hemoglobin, a NO chelator, and 5, 5- dimethyl-L-pyrroline-N-oxide(DMPO), an electron spin trap, inhibited $[^3H]NE$ release dose-dependently. Ischemia-evoked $[^3H]NE$ release was inhibited by methylene blue, a soluble guanylate cyclase inhibitor, and potentiated by 8-bromo-cGMP, a cell permeable cGMP analog, zaprinast, a cGMP phosphodiesterase inhibitor, and S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide generator. These results suggest that the ischemia-evoked $[^3H]NE$ release is mediated by NMDA receptors, and activation of NO system is involved.

• Physical Therapy Korea
• /
• v.17 no.1
• /
• pp.69-76
• /
• 2010

Ischemia that causes stroke induces inflammation of brain cells and apoptosis and as a result, it influences much on the functional part of a man. The needle electrode electrical stimulation (NEES) that combines acupuncture of oriental medicine with electric therapy of western medicine relieves inflammation of cells and has effect on regrowth of nerve tissues. This study was conducted to verify the influence of NEES on the occurrence of c-Fos of cerebrum after applying NEES to the meridian point, Zusanli (ST 36) of a rats with induced ischemia. Global ischemia was induced by using ligation method on common carotid artery of male Sprague Dawley (SD) rats. The ligation was maintained for 5 minutes and then suture was removed for blood reperfusion. After inducing global ischemia, NEES was done to the left and right meridian points of Joksamri of a rat for 30 minutes after 12 hours, 24 hours, and 48 hours. The findings were as follows. 1. In the result of immunohistochemical method, the number of c-Fos immune response cells significantly decreased (P<.05) in NEES group than the control group (GI) that did not get NEES. 2. In the result of western blotting, the occurrence of c-Fos after 24 hours from the inducement of ischemia significantly decreased (P<.05) in NEES group than the control group (GI) that did not get NEES. Therefore, as the effect of NEES was shown highest after 24 hours from the ischemia, it is suspected that NEES would take important role in early treatment after cerebral stroke.

• The Journal of Internal Korean Medicine
• /
• v.30 no.3
• /
• pp.612-623
• /
• 2009

Objectives : The water extract of Sopung-tang (SPT) has been traditionally used in the treatment of acute stroke in Oriental Medicine. Pro-inflammatory cytokines play a critical role in the onset of post-ischemic inflammatory cascades. The present study was designed to investigate the effects of SPT on pro-inflammatory cytokine production in a photothrombotic ischemia mouse model. Methods : After SPT oral administration to the mice for five days, with using Rose Bengal and cold light, photothrombotic ischemia lesion was induced in stereotactically held male BALB/c mice. Also, results including, gross finding lesion size, histopathological finding changes, and inflammatory cytokine expression changes from the photothrombotic ischemia mouse model were observed. Results : The photothrombotic ischemia lesion was decreased by the oral injection of SPT. Also, SPT inhibited the expression of TNF-$\alpha$, IL-$1{\beta}$, IL-6, the active form of caspase-3 protease, and transglutaminase-2 in the photothrombotic ischemia lesion. Conclusions : These results suggest that SPT protects the ischemic death of brain cells through suppression of the production of anti-inflammatory cytokines and catalytic activation of caspase-3 protease in the photothrombotic ischemia mouse model.

• Proceedings of the Korean Society of Applied Pharmacology
• /
• 1994.04a
• /
• pp.340-340
• /
• 1994

Since total hepatic ischemia(IS) occurs with transplantation, there has been interest in evaluating hepatic function after ischemia and subsequent reflow of blood. Four groups of animals were studied: group 1 (sham), group 2 (30mins IS), group 3 (60mins IS), and g.cup 4 (90mins IS). Serum transaminase(STA), wet weight-to-dry weight ratio(W/D), lipid peroxides(LPO), glucose-6-phosphatase(G-6-Pase) activity, Na$\^$+//K$\^$+/-ATPase(ATPase) activity were measured at 1, 5 and 24hrs after hepatic ischemia. Significant changes occurred between 1 and 5hrs of reperfusion. STA was 3579${\pm}$401, 4593${\pm}$675 and 6348${\pm}$808 U/L in group 2, 3 and 4 respectively. These changes were ischemic time-dependent manner. W/D in group 3 and 4 were significantly increased than that in sham group at all time points measured. In sham group, the level of LPO in the liver microsome remained constant at approximately 0. 5nmole MDA formed/mg protein througllout the experiment, In all ischemic groups on the other hand, the level of LPO started to increase at ischemia and markedly increased at all reperfusion period. Similar to STA, these changes were also dependent on duration of ischemia. Although G-6-Pase activity remained unchanged in both group 2 and group 3 until 5hrs of reperfusion, marked decrease in G-6-Pase activity was observed at grcup 4. ATPase activity was significantly decreased at 1, 5 and 24 hrs of reperfusion in group 3, whereas it was not changed in group 2. Furthermore, ATPase activity in group 4 started to decrease at ischemia and markedly decreased for entire reperfusion period. These data suggest that severity of hepatocellular injury is associated with period of ischemia as well as period of reperfusion.

• The Korean Journal of Physiology and Pharmacology
• /
• v.11 no.2
• /
• pp.45-55
• /
• 2007

We elucidated the effects of various components of ischemic medium on the outcome of simulated ischemia-reperfusion injury. Hypoxia for up to 12 hours induced neither apoptotic bodies nor LDH release. However, reoxygenation after 6 or 12 hours of hypoxia resulted in a marked LDH release along with morphological changes compatible with oncotic cell death. H9c2 cells were then subjected to 6 hours of simulated ischemia by exposing them to modified hypoxic glucose-free Krebs-Henseleit buffer. Lowered pH (pH 6.4) of simulated-ischemic buffer resulted in the generation of apoptotic bodies during ischemia, with no concomitant LDH release. The degree of reperfusion-induced LDH release was not affected by the pH of ischemic buffer. Removal of sodium bicarbonate from the simulated ischemic buffer markedly increased cellular damages during both the simulated ischemia and reperfusion. Addition of lactate to the simulated ischemic buffer increased apoptotic cell death during the simulated ischemia. Most importantly, concomitant acidosis and high lactate concentration in ischemic buffer augmented the reperfusion-induced oncotic cell death. These results confirmed the influences of acidosis, bicarbonate deprivation and lactate on the progression and outcome of the simulated ischemia-reperfusion, and also demonstrated that concomitant acidosis and high lactate concentration in simulated ischemic buffer contribute to the development of reperfusion injury.

• The Korean Journal of Physiology
• /
• v.6 no.2
• /
• pp.9-17
• /
• 1972

This experiment was carried out to investigate systematically how the aerobic metabolic capacity of renal tissue reduced by the effects of a period of induced ischemia. Aerobic metabolic studies were performed on homogenates of cortex and medulla of rabbits. Ischemia was induced by occluding the renal vein or renal artery of the left kidney for an hour. The right kidney used as a paired control. Aerobic metabolism was asesssed by measuring the oxygen consumption using the Warburg's manometric apparatus. The results are summarized as follows: 1. One hour of occlusive ischemia does not increase in the kidney weight in the renal arterial occlusion but increase in the renal venous occlusion. 2. Occlusion of either the renal vein or renal artery for an hour did not reduce to any significant degree the level of endogenous substrate in cortical homogenates as measured the rates of $0_2$ consumption. 3. A significant reduction in the rate of $C_2$ consumption was noted in the medullary homogenates of renal venous occluded kidneys while renal arterial occlusion had less of an effect. 4. The capaciy of homogenates for aerobic metabolism is not reduced by acute ischemia, because of the higher rate of oxygen consumption induced by exogenous glucose in renal vein occlusion. 5. The oxygen consumption of medullary homogenate more decreased to acute ischemia than cortical homogenates. The results of this investigation suggest that one hour circulatory stasis does not reduce major potential capacity of renal cortical tissue at the subcellular level to produce energy. In contrast, the aerobic metabolism of medullary tissue is reduced by renal ischemia. Further, both cortex and medulla appear to be more sensitive to ischemia induced by renal venous occlusion than by renal arterial occlusion.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.17 no.3
• /
• pp.791-797
• /
• 2003

This study investigated the effect of Yanggyuksanhwa-tang on cerebral ischemia of the rats. Considering age-related impact on cerebral ischemia, aged rats (18 months old) were used for this study. Ischemic damage was induced by the transient occlusion of bilateral common carotid arteries (BCAO) under the hypotension. Yanggyuksanhwa-tang was administered twice orally. Then changes of pyramidal neurons and heat shock protein 72 (HSP72) expressions in ischemic damaged hippocampus were of observed. The BCAO in aged rats led significant decrease of pyramidal neurons in CA1 hippocampus. While the treatment of Yanggyuksanhwa-tang significantly attenuated the reduction of pyramidal neurons in CA1 hippocampus following BCAO ischemia. The BCAO in aged rats led significant increase of HSP72 expression in CA1 and mild in CA3 hippocampus. While the treatment of Yanggyuksanhwa-tang significantly attenuated the increase of HSP72 expression in CA1 hippocampus following BCAO ischemia. The extent of HSP72 expression in CA2 and DG of hippocampus was not different between the sham operated group, the BCAO ischemia control group, and the group of Yanggyuksanhwa-tang administration after BCAO ischemia. The treatment of Yanggyuksanhwa-tang significantly attenuated the increase of normalized optical density depending on HSP72 expression in CA1 hippocampus following BCAO ischemia.