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Citicoline Protects Against Cognitive Impairment in a Rat Model of Chronic Cerebral Hypoperfusion
이현준,강지승,김영인,강지승 대한신경과학회 2009 Journal of Clinical Neurology Vol.5 No.1
Background and PurposeaaCerebral white matter (WM) lesions are frequently observed in human cerebrovascular diseases, and are believed to be responsible for cognitive impairment. Various neuroprotective agents can suppress this type of WM or neuronal damage. In this study, we investigated whether citicoline, a drug used to treat acute ischemic stroke, can attenuate WM lesions and cognitive decline caused by chronic hypoperfusion in the rat. MethodsaaAnimals were divided into immediate- and delayed-treatment groups. Those in the immediate-treatment group received a sham operation, citicoline (500 mg/kg/day), or phosphate buffered saline (PBS) treatment. Citicoline or PBS was administered intraperitoneally for 21 days after occluding the bilateral common carotid arteries. Rats in the delayed-treatment group were intraperitoneally administered with either 500 mg/kg/day citicoline or PBS for 21 days beginning on the 8th day after the operation. From the 17th day of administration, the rats were placed in an eight-arm radial maze to examine their cognitive abilities. After completing the administration, tissues were isolated for Klüver-Barrera and the terminal deoxynucleotidyl transferase biotin-dUTP nick end labelling (TUNEL) staining. ResultsaaIn the immediate-treatment group, cognitive functions were preserved in the citicolinetreated group, and WM damage and TUNEL-positive cells differed significantly between the citicoline- and PBS-treated animals. In the delayed-treatment group, there was no decrease in WM damage and TUNEL-positive cells, but cognitive improvement was evident for citicoline treatment relative to PBS treatment. ConclusionsaaThese results show that citicoline can prevent WM damage and aid cognitive improvement, even after a certain extent of disease progression. Citicoline might be useful in patients with acute ischemic stroke as well as in chronic stroke accompanied with cognitive impairment.
이현준,이승기,Lee, Hyun-Jun,Lee, Seung-Ki Korean Society for Biochemistry and Molecular Biol 1990 한국생화학회지 Vol.23 No.3
간의 재생기간 중 감마인터페론의 LDH A 유전자 발현에 대한 억제효과에 대하여 연구하였다. 또한 간 부분 절제 후 감마인터페론에 의한 LDHA 유전자와 DNA 합성억제가 cAMP에 의해 매개될 가능성을 검토하였다. 감마인터페론을 간 부분절제 20시간 전에 쥐 100g당 $1{\times}10^4$ IU의 양으로 복강내 투여하였을 때 간 부분절제 후 21시간에서의 LDH A mRNA 농도와 24시간에서의 DNA 합성을 억제시켰다. Dibutyryl cAMP를 간 부분절제 후 8-12시간에 쥐 100g당 0.5mg의 양으로 복강내 투여하였을 때 감마인터페론에 의해 억제된 LDH A mRNA의 농도와 DNA 합성을 회복시켰다. 그러나 감마인터 페론은 재생간의 cAMP 농도에는 영향을 미치지 않았다. 이상의 결과와 다른 연구결과로부터 간 재생기간 중 감마인터페론의 LDH A 유전자 발현과 DNA 합성에 대한 억제효과는 cAMP에 의해 매개되지 않고 c-myc protooncogene의 발현억제에 의한 효과일 가능성을 제시하고자 한다. We studied the inhibitory effect of ${\gamma}$-interferon on the expression of LDH A gene at the transcriptional level during regeneration of rat liver. Also, we examined the possible involvement of cAMP as a second messenger for the inhibition of LDH A gene expression and DNA synthesis by ${\gamma}$-interferon after partial hepatectomy of rat. ${\gamma}$-interferon ($1{\times}10^4$IU/100g of rat. i.p.) injected at 20 h prior to partial hepatectomy reduced LDH A mRNA concentration at 21 h and inhibited DNA synthesis at 24 h after the partial hepatectomy. Dibutyryl cAMP (0.5 mg/100 g of rat, i.p.) injected at 8-12 h after partial hepatectomy restored both the LDH A mRNA concentration and the DNA synthetic activities which were inhibited by ${\gamma}$-interferon. However, ${\gamma}$-interferon did not affect the cAMP levels determined by RIA method in regenerating rat liver. The above results suggest that during regeneration of rat liver, the inhibitory effects of ${\gamma}$-interferon on the induction of LDH A gene transcription and the DNA synthesis, both of which activities were reported to be regulated by cAMP, may not be mediated by cAMP, but may be mediated by the inhibition of c-myc protooncogene expression.