• 제목/요약/키워드: Brain damage

검색결과 686건 처리시간 0.032초

LPS와 PMA에 손상된 신경교세포에 대한 뇌혈전방의 방어효과 (Protective Effects of Nueihyuljunbang on LPS Combined PMA Induced Cytotocity in C6 Gilal Cell)

  • 서관수;문병순;성강경;임규상;신선호
    • 대한한의학회지
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    • 제22권3호
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    • pp.1-10
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    • 2001
  • Objectives : The water extract of Nueihyuljunbang (NHJB) has long been used for treatment of ischemic brain damage in Oriental Medicine. However, little is known about the mechanism by which the water extract of NHJB recovers brain cens from ischemic damage. Methods : To elucidate the protective mechanism on ischemic induced cytotoxicity, we investigated the regulation of lipopolysaccharide (LPS) and phorbol-12-myristate-13-acetate (PMA)-induced inducible nitric oxide synthase (iNOS) expression in C6 glial cells. Results : LPS combined PMA treatment for 72 hours in C6 glial cells markedly induced nitric oxide (NO), but treatment of the cells with the water extract of NHJB decreased dose-dependently nitrite formation. In addition, LPS combined PMA treatment for 72 hours induced severe celt death and lactate dehydrogenase (LDH) release in C6 glial cells. However, treatment of the celts with the water extract of NHJB did not induce significant change compared to control cells. Furthermore, the protective effects of the water extract of NHJB were mimicked by the treatment of NGMMA, a specific inhibitor of NOS. LPS combined PMA induced iNOS activation in C6 glial cells caused chromosomal condensation and fragmentation of the nuclei by caspase activation. The treatment of C6 glial cells with the water extract of NHJB might suppress apoptosis via caspase inhibition by regulation of iNOS expression. Conclusions : From the results, we suggest that the protective effects of the water extract of NHJB against ischemic brain damage may be mediated by regulation of iNOS during ischemic condition.

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광두근(廣豆根) 분획물이 중대뇌동맥폐쇄(中大腦動脈閉鎖)에 의한 뇌허혈손상에 미치는 효과(I) - 행동평가를 기준으로 (Effect of Sophora Subprostrata Fractions on Focal Ischemic Brain Damage Induced by Middle Cerebral Artery Occlusion in Rats(I))

  • 최문석;김연섭
    • 동의생리병리학회지
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    • 제19권3호
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    • pp.760-764
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    • 2005
  • This research was performed to investigate protective effect of Sophora Subprostrata fractions against focal ischemic brain damage after middle cerebral artery(MCA) occlusion. Rats were divided into six groups: MCA-occluded group(Control); each administered groups with Sophora Subprostrata total phase(Total), Sophora Subprostrata Aqueous phase (Aqueous), Sophora Subprostrata BuOH phase(BuOH), and Sophora Subprostrata Alkaloid phase(Alkaloid) after MCA-occlusion; sham-operated group(Sham). The right MCA was occluded by A poly-L-lysine coated 4-0 nylon suture thread through the internal carotid artery permanently. Sophora Subprostrata and fractions were administered orally(5mg/ml) for 7 days after MCA-occlusion. The behavior of ischemic rats were examined at 24 hours, 3, 5 and 7 days after MCA-occlusion from the views of 4 different aspects: posture & balance tests(4 subtests), reflex tests(6 subtests), muscle-tone tests(3 subtests), and foot-fault test. The results showed that 1) in muscle tone test, Sophora Subprostrata total phase only increased reduced muscle tone function from 3 to 7 days, 2) in reflex test, Sophora Subprostrata total and Aqueous phase increased fast recovery from 24 hours and 3 days, 3) in posture & balance test, Sophora Subprostrata total and Aqueous phase increased fast recovery from 24 hours, and Sophora Subprostrata BuOH and Alkaloid phase increased posture & balance function from 3 days, but 4) in motor function test, Sophora Subprostrata did not show effective recovery compared with control group. In conclusion, Sophora Subprostrata has protective effects against brain damage at the early stage of focal cerebral ischemia. Sophora Subprostrata total and Aqueous phase produced more pronounced protective effect against focal ischemic brain damage.

속명탕(續命湯)이 C6 glial cell 보호 및 허혈성 뇌손상에 미치는 영향 (Effects of Sokmyeung-tang(SMT) on the Protection of C6 Glial Cells and Ischemic Brain Damage)

  • 안가영;최은희;김인수;강성순;이영수;홍석;전상윤
    • 대한한방내과학회지
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    • 제32권1호
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    • pp.43-55
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    • 2011
  • Objectives : Sokmyeung-tang(SMT) has been used for treatment of CVA in traditional oriental medicine, so this study was designed to evaluate the effect of SMT's protection on brain cell damage against the oxidative stress that was affected by CVA, We also investigated the effect of motor function improvement and neurotrophic factor in ischemic cerebral damaged rats. Methods : We measured cell viability after administrating SMT, chemicals(Paraquat, SNP, rotenone, and $H_2O_2$) which cause oxidative stress, and both SMT and chemicals. We carried out neurobehavioral evaluation(Rotarod test, Beam-walking test, postural reflex test) and observed BDNF (brain-derived neurotrophic factor) expression by injecting SMT into ischemic cerebral damaged rat. Results : Through this study, we observed the following three results. First, brain cell death caused by paraquat, rotenone, and $H_2O_2$ significantly decreased with the treatment of SMT. Second, neuronal movement function in ischemic cerebral damaged rats was significantly improved by the treatment of SMT. Third, BDNF in ischemic cerebral damaged rats increased with the treatment of SMT. Conclusions : SMT protects brain cells from damage induced by oxidative stress (Paraquat, rotenone, $H_2O_2$). SMT also improves neuronal movement function and increases BDNF in ischemic cerebral damaged rats.

Ginsenoside compound K reduces the progression of Huntington's disease via the inhibition of oxidative stress and overactivation of the ATM/AMPK pathway

  • Hua, Kuo-Feng;Chao, A-Ching;Lin, Ting-Yu;Chen, Wan-Tze;Lee, Yu-Chieh;Hsu, Wan-Han;Lee, Sheau-Long;Wang, Hsin-Min;Yang, Ding-I.;Ju, Tz-Chuen
    • Journal of Ginseng Research
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    • 제46권4호
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    • pp.572-584
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    • 2022
  • Background: Huntington's disease (HD) is a neurodegenerative disorder caused by the expansion of trinucleotide CAG repeat in the Huntingtin (Htt) gene. The major pathogenic pathways underlying HD involve the impairment of cellular energy homeostasis and DNA damage in the brain. The protein kinase ataxia-telangiectasia mutated (ATM) is an important regulator of the DNA damage response. ATM is involved in the phosphorylation of AMP-activated protein kinase (AMPK), suggesting that AMPK plays a critical role in response to DNA damage. Herein, we demonstrated that expression of polyQ-expanded mutant Htt (mHtt) enhanced the phosphorylation of ATM. Ginsenoside is the main and most effective component of Panax ginseng. However, the protective effect of a ginsenoside (compound K, CK) in HD remains unclear and warrants further investigation. Methods: This study used the R6/2 transgenic mouse model of HD and performed behavioral tests, survival rate, histological analyses, and immunoblot assays. Results: The systematic administration of CK into R6/2 mice suppressed the activation of ATM/AMPK and reduced neuronal toxicity and mHTT aggregation. Most importantly, CK increased neuronal density and lifespan and improved motor dysfunction in R6/2 mice. Conversely, CK enhanced the expression of Bcl2 protected striatal cells from the toxicity induced by the overactivation of mHtt and AMPK. Conclusions: Thus, the oral administration of CK reduced the disease progression and markedly enhanced lifespan in the transgenic mouse model (R6/2) of HD.

주기편측간질모양방전은 발작현상이 아니라 단지 급성 뇌손상을 반영하는 것이다 (Periodic Lateralized Epileptiform Discharges Are Not Ictal Phenomenon, and Just Reflect an Acute Brain Damage)

  • 이상암
    • Annals of Clinical Neurophysiology
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    • 제13권1호
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    • pp.26-30
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    • 2011
  • Although the pathophysiologic mechanism is unknown, there has been long-running debate on whether periodic discharges such as periodic lateralized epileptiform discharges (PLEDs) and generalized periodic epileptiform discharges are an ictal or interictal EEG pattern. The goal of this review is to give evidence that such periodic discharges on EEG are not ictal phenomenon and just represent underlying acute brain damage. This review includes coma with epileptiform EEG pattern and its prognostic and therapeutic implications. Based on previous reports, rather than taking the view PLEDs represent either an underlying ictal process or an electrographic correlate of neuronal injury, it would be more reasonable that PLEDs are considered as a dynamic pathophysiological state in which unstable neurobiological processes create an ictal-interictal continuum.

일시적 국소 뇌허혈 흰쥐모델에서 원지석창포산의 뇌손상 및 인지기능 보호효과 (Protective Effects Wonjiseokchangpo-san has on Brain Damage and Cognitive Dysfunction in Transient Focal Cerebral Ischemia)

  • 강미선;장규태;김장현
    • 동의생리병리학회지
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    • 제18권6호
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    • pp.1777-1783
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    • 2004
  • This study was conducted to determine the effects Wonjiseokchangpo-san on brain damage in transient focal cerebral ischemia. Rats were used for testing in the following three models: Morris Water Maze, Eight-Arm Radial Maze, and Histochemistry. In the Morris Water Maze Model, the Wonjiseokchangpo-san group showed significant decrease in the 3rd and 6th training session compared with the ischemia group. A retention test, in the Morris Water Maze Model, was performed on the 7th day without the escape platform. The Wonjiseokchangpo-san group showed significant increase compared to the ischemia group. In the Eight-Arm radial Maze model, the Wonjiseokchangpo-san group showed significant decrease in the error rate compared to the ischemia group. In the density of hippocampal CA1 cell of the cresyl violet-stained section, the Wonjiseokahangpo-san group showed significant increase compared to the ischemia group. These results suggest that Wonjiseokchangpo-san may have a significant protective effect on brain damage and cognitive dysfunction in transient focal cerebral ischemia.

일시적 국소 뇌허혈 흰쥐모델에서 거풍지보단의 뇌손상 및 인지기능 보호효과 (Protective Effects of Geupunggibodan on Brain Damage and Cognitive Dysfunction in Transient Focal Cerebral Ischemia in Rats)

  • 정성욱;장규태;김장현
    • 대한한의학회지
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    • 제26권2호
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    • pp.52-62
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    • 2005
  • Objectives: This study was conducted to determine the effects of Geupunggibodan on brain damage in transient focal cerebral ischemia in rats. Methods: Rats were used for testing in the following three models: Morris water maze, eight-ann radial maze, and histochemistry. Results: In the Morris water maze model, the Geupunggibodan group showed significant decrease in the 3rd, 4th and 6th training sessions compared with the ischemia, group. A retention test in the Morris water maze model was performed on the 7th day without the escape platform. The Geupunggibodan group showed significant increase compared to the ischemia group. In the eight-ann radial maze model, the Geupunggibodan group showed significant decrease in the error rate compared to the ischemia group. In the density of hippocampal CA1 cell of the cresyl violet-stained section, the Geupunggibodan group showed significant increase compared to the ischemia group. Conclusions: These results suggest that Geupunggibodan may have a significant protective effect on brain damage and cognitive dysfunction in transient focal cerebral ischemia.

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Lysophosphatidic Acid Receptor 1 Plays a Pathogenic Role in Permanent Brain Ischemic Stroke by Modulating Neuroinflammatory Responses

  • Supriya Tiwari;Nikita Basnet;Ji Woong Choi
    • Biomolecules & Therapeutics
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    • 제32권3호
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    • pp.319-328
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    • 2024
  • Lysophosphatidic acid receptor 1 (LPA1) plays a critical role in brain injury following a transient brain ischemic stroke. However, its role in permanent brain ischemic stroke remains unknown. To address this, we investigated whether LPA1 could contribute to brain injury of mice challenged by permanent middle cerebral artery occlusion (pMCAO). A selective LPA1 antagonist (AM152) was used as a pharmacological tool for this investigation. When AM152 was given to pMCAO-challenged mice one hour after occlusion, pMCAO-induced brain damage such as brain infarction, functional neurological deficits, apoptosis, and blood-brain barrier disruption was significantly attenuated. Histological analyses demonstrated that AM152 administration attenuated microglial activation and proliferation in injured brain after pMCAO challenge. AM152 administration also attenuated abnormal neuroinflammatory responses by decreasing expression levels of pro-inflammatory cytokines while increasing expression levels of anti-inflammatory cytokines in the injured brain. As underlying effector pathways, NF-κB, MAPKs (ERK1/2, p38, and JNKs), and PI3K/Akt were found to be involved in LPA1-dependent pathogenesis. Collectively, these results demonstrate that LPA1 can contribute to brain injury by permanent ischemic stroke, along with relevant pathogenic events in an injured brain.

외상성 뇌손상환자에서 Amantadine의 사용 (The use of Amantadine in Traumatic Brain Injury Patients)

  • 정한용;김양래
    • 생물정신의학
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    • 제7권1호
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    • pp.55-63
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    • 2000
  • Avariety of symptoms can occur following traumatic brain injury(TBI) or other types of acquired brain injury. These symptoms can include problems with short-term memory, attention, planning, problem solving, impulsivity, disinhibition, poor motivation, and other behavioral and cognitive deficit. These symptoms may respond to certain drugs, such as dopaminergic agents. Amantadine may protect patients from secondary neuronal damage after brain injury as a effect of NMDA receptor antagonists and may improve functioning of brain-injured patients as a dopaminergic agonist. Clinically, based on current evidence, amantadine may provide a potentially effective, safe, and inexpensive option for treating the cognitive, mood, and behavioral disorders of individuals with brain injury. The rationales for using amantadine are discussed, and pertinent literatures are reviewed.

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In vivo evidence for brain-to-blood efflux transport of taurine and regulation of this transport by tumor necrosis factor-$\alpha$ at the blood-brain barrier

  • Lee, Na-Young;Kang, Young-Sook
    • 대한약학회:학술대회논문집
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    • 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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    • pp.69.2-69.2
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    • 2003
  • The purpose of this study is to examine whether the efflux system for taurine from brain to blood is present on the blood-brain barrier (BBB) using the brain efflux index (BEl) method and taurine transport system is regulated by CNS cell damage with oxidative stress agent such as diethyl maleate (DEM) or tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) in vivo. [$^3$H]Taurine was microinjected into parietal cortex area 2 (Par2) of the rat brain, and was eliminated from the brain with efflux transport rate of 1.22 10$\^$-2//min, and the process is saturable with a $K_{m}$ of 43.5 ${\mu}$M. (omitted)

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