• The Korea Journal of Herbology
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• v.27 no.6
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• pp.71-76
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• 2012

Objectives : The purpose of this study was to evaluate the neuroprotective effect of Pueraria lobata extract on focal cerebral ischemia in mice. Methods : Focal cerebral ischemia was induced by occlusion of the right middle cerebral artery using the intraluminal filament model. ICR male mice underwent 90 minutes of middle cerebral artery occlusion (MCAo) followed by 24 hours of reperfusion. Mice were administered Pueraria lobata extract orally at the dose of 300mg/kg just prior to reperfusion. Rotarod test and balance beam test were practiced to assess sensory-motor function 23 hours after MCAo. In rotarod test, the latency to fall on the accelerating rotarod was recorded for 5 min. In balance beam test, the score was graded according to number of slips and latency to cross. The infarct volume was measured 24 hours after MCAo using 2% 2,3,5-triphenyltetrazolium chloride (TTC) staining. Results : Pueraria lobata extract treated group showed significant reduction in infarct volume by 27.3% compared to control group (p<0.05). In rotatod test, it also showed significant extension of latency time compared to control group ($67.82{\pm}15.08$ vs. $5.62{\pm}1.06$, p<0.001). In contrast to performance in rotarod test, that in balance beam test did not improve with Pueraria lobata extract treatment. Conclusions : We conclude that Pueraria lobata extract has a significant neuroprotective effect and reduces damage of sensory-motor function in MCAo model. These findings suggest that Pueraria lobata could be a potent neuroprotective agent.

• The Korean Journal of Pain
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• v.32 no.2
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• pp.79-86
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• 2019

Background: The use of aroma oils dates back to at least 3000 B.C., where it was applied to mummify corpses and treat the wounds of soldiers. Since the 1920s, the term "aromatherapy" has been used for fragrance therapy with essential oils. The purpose of this study was to determine whether the essential oil of Eucalyptus (EOE) affects pain pathways in various pain conditions and motor coordination. Methods: Mice were subjected to inhalation or intraperitoneal injection of EOE, and its analgesic effects were assessed by conducting formalin, thermal plantar, and acetic acid tests; the effects of EOE on motor coordination were evaluated using a rotarod test. To determine the analgesic mechanism, 5'-guanidinonaltrindole (${\kappa}$-opioid antagonist, 0.3 mg/kg), naltrindole (${\delta}$-opioid antagonist, 5 mg/kg), glibenclamide (${\delta}$-opioid antagonist, 2 mg/kg), and naloxone (${\mu}$-opioid antagonist, 4, 8, 12 mg/kg) were injected intraperitoneally. Results: EOE showed an analgesic effect against visceral pain caused by acetic acid (EOE, 45 mg/kg); however, no analgesic effect was observed against thermal nociceptive pain. Moreover, it was demonstrated that EOE did not have an effect on motor coordination. In addition, an anti-inflammatory effect was observed during the formalin test. Conclusions: EOE, which is associated with the ${\mu}$-opioid pain pathway, showed potential effects against somatic, inflammatory, and visceral pain and could be a potential therapeutic agent for pain.

• Biomolecules & Therapeutics
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• v.6 no.4
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• pp.406-411
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• 1998

The pre-mixed $_{13}C$-urea powder preparation in ${Helikit}_{TM}$ for test of Helicobacter pylori was evaluated for pharmacological properties. The oral doses of the preparation used in mice were 30-fold as compared to human doses. The results obtained in the present study demonstrate that spontaneous movement, hexobarbital-induced hypnosis, rotarod performance, body temperature, acetic acid-induced writhing syndrome, chemical and electroshock convulsion, pupil size and intestinal propulsion had not been affected at the oral doses of 230, 700 and 2100 mg/kg in mice. The blood pressure was slightly elevated as given intravenously in rats at a dose of 5 mg/kg of the preparation, but respiration was not influenced at the dose. In isolated guinea pig ileum and rat fundus preparation, the preparation at a concentration of $1{\times}10^{4}$ g/ml neither caused any direct effect nor inhibited the contraction produced by acetylcholine, histamine or 5-hydroxytryptamine. These results reported here provide evidence that pre-mixed $^{13}C$ 13/C-urea powder preparation is free of general pharmacological properties performed in oral administration.

• Journal of Korean Neurosurgical Society
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• v.38 no.1
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• pp.41-46
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• 2005

Objective : A study of the histopathologic and neurobehavioral correlates of cortical impact injury produced by increasing impact velocity using the controlled cortical impact[CCI] injury model is studied. Methods : Twenty-four Sprague-Dawley rats [$200{\sim}250g$] were given CCI injury using a pneumatically driven piston. Effect of impact velocity on a 3mm deformation was assessed at 2.5m/sec [n=6], 3.0m/sec [n=6], 3.5m/sec [n=6], and no injury [n=6]. After postoperative 24hours the rats were evaluated using several neurobehavioral tests including the rotarod test, beam-balance performance, and postural reflex test. Contusion volume and histopathologic findings were evaluated for each of the impact velocities. Results : On the rota rod test, all the injured rats exhibited a significant difference compared to the sham-operated rats and increased velocity correlated with increased deficit [p<0.001]. Contusion volume increased with increasing impact velocity. For the 2.5, 3.0, and 3.5m/sec groups, injured volumes were $18.8{\pm}2.3mm^3$, $26.8{\pm}3.1mm^3$, and $32.5{\pm}3.5mm^3$, respectively. In addition, neuronal loss in the hippocampal sub-region increased with increasing impact velocity. In the TUNEL staining, all the injured groups exhibited definitely positive cells at pericontusional area. However, there were no significant differences in the number of positive cells among the injured groups. Conclusion : Cortical impact velocity is a critical parameter in producing cortical contusion. Severity of cortical injury is proportional to increasing impact velocity of cortical injury.

• Journal of the Korean Society of Food Science and Nutrition
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• v.43 no.6
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• pp.799-806
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• 2014

The present study was conducted to evaluate the effects of extract from Eriobotrya japonica leaves (EJE) on cognitive impairment induced by scopolamine, a muscarinic antagonist, in rats. Scopolamine injection (1 mg/kg, i.p.) impaired performance in rats in the passive avoidance test as well as in water maze test and severely reduced cholinergic system reactivity, as indicated by reduced acetylcholine levels and increased acetylcholinesterase activity. Daily administration of EJE significantly increased step-through latency in the passive avoidance test, reduced escape latency, and increased time spent in the platform quadrant in the Morris water maze test. EJE protected against scopolamine-induced cholinergic system deficit, including reduced acetylcholine levels and increased acetylcholinesterase activity in whole brain homogenates. These results suggest that EJE provides a significant anti-amnesic effect against scopolamine-induced cholinergic system deficits and cognitive impairment.

• Journal of Korean Neurosurgical Society
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• v.39 no.2
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• pp.130-135
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• 2006

Objective : After ischemic stroke, partial recovery of function frequently occurs and may depend on the plasticity of axonal connections. Here, we examine whether blockade of the Nogo/NogoReceptor[NgR] pathway might enhance axonal sprouting and thereby recovery after focal brain infarction. Methods : Adult male Sprague Dawley rats weighing $250{\sim}350g$ were used. Left middle cerebral artery occlusion[MCAO] was induced with a intraluminal filament. An osmotic mini pump [Alzet 2ML4, Alza Scientific Products, Palo Alto, CA] for the infusion of NgR-Ecto[310]-Fc to block Nogo/NgR pathway was implanted 1 week after cerebral ischemia. Prior to induction of ischemia, all animals received training in the staircase and rotarod test. Two weeks after biotin dextran amine injection, animals were perfused transcardially with PBS, followed by 4% paraformadehyde/PBS solution. Brain and cervical spinal cord were dissected. Eight coronal sections spaced at 1mm intervals throughout the forebrain of each animal with cresyl violet acetate for determination of infarction size. Images of each section were digitized and the infarct area per section was measured with image analysis software. Results : Histological examination at 11 weeks post-MCAO demonstrates reproducible stroke lesions and no significant difference in the size of the stroke between the NgR[310]Ecto-Fc protein treated group and the control group. Behavioral recovery is significantly better and more rapid in the NgR-Ecto[310]-Fe treated group. Blockade of NgR enhances axonal sprouting from the uninjured cerebral cortex and improves the return of motor task performance. Conclusion : Pharmacological interruption of NgR allows a greater degree of axonal plasticity in response this is associated with improved functional recovery of complicated motor tasks.

• Annals of Clinical Neurophysiology
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• v.7 no.2
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• pp.101-106
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• 2005

Background: There is no currently effective treatment for amyotrophic lateral sclerosis (ALS), although this disorder is a progressive neurodegenerative disease resulting in death within several years. Because recent evidence suggests that homocysteine (HC) is highly related to neurodegenerative disorders with aging, we tried to elucidate the effects of multi-vitamin therapy on G93A SOD1 transgenic mice. Methods: We treated this murine model of ALS with multi-vitamin (folic acid 1.97 mg/day, pyridoxine 0.98 mg/day, cyanocobalamin 0.1 mg/day) from 45 days of age, per oral. We performed the rotarod test from postnatal $10^{th}$ week, weekly. Results: We found that multi-vitamin reinforcement significantly prolonged average lifespan and delayed disease onset with improvement of motor performance. However, it did not significantly slow disease progression and statistical differences of weight loss were not observed between in transgenic mice and controls. Conclusions: These results suggest that multi-vitamin can be a potent therapeutic strategy for familial forms of ALS.