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Choi, In-Young,Hwang, Lakkyong,Jin, Jun-Jang,Ko, Il-Gyu,Kim, Sung-Eun,Shin, Mal-Soon,Shin, Key-Moon,Kim, Chang-Ju,Park, Sung-Wook,Han, Jin-Hee,Yi, Jae-Woo D.A. Spandidos 2017 Experimental and therapeutic medicine Vol.13 No.1
<P>Cerebral ischemia results from cerebrovascular occlusion, which leads to neuronal cell death and eventually causes neurological impairments. Dexmedetomidine is a potent and highly selective α<SUB>2</SUB>-adrenoreceptor agonist with actions such as sedation, anxiolysis, analgesia and anesthetic-sparing effects. We investigated the effect of dexmedetomidine on apoptosis in the hippocampus after transient global ischemia in gerbils. Transient global ischemia was induced by ligation of both common carotid arteries. Dexmedetomidine was administrated intraperitoneally at three respective doses (0.1, 1 and 10 µg/kg) once per day for 14 consecutive days beginning a day after surgery. Short-term memory was assessed by use of a step-down avoidance task. Apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling assay, immunohistochemistry for caspase-3, and western blot analysis of Bcl-2-associated X protein, B-cell lymphoma 2, Bid, cytochrome <I>c</I>, apoptotic protease activating factor-1 and caspase-9 in the hippocampus. Induction of global ischemia deteriorated short-term memory by enhancing the expression of apoptosis-related molecules in the hippocampus. Treatment with dexmedetomidine suppressed the expression of apoptosis-related molecules under ischemic conditions, resulting in short-term memory improvement. Under normal conditions, dexmedetomidine exerted no significant effect on apoptosis in the hippocampus. The present results suggest that the α<SUB>2</SUB>-adrenoceptor agonist dexmedetomidine may be a useful therapeutic agent for the treatment of ischemic brain diseases.</P>
Sang-Hak Lee,Jun-Jang Jin,Lakkyong Hwang,Sung-Eun Kim,Chang-Ju Kim,Il-Gyu Ko 한국운동재활학회 2015 한국운동재활학회 학술대회 Vol.2015 No.10
Cerebral ischemia results from cerebrovascular occlusion, which leads to neuronal cell death and eventually causes neurological disorders. Cordyceps is a known to have variable actions, such as increasing sexual drive, improving renal function, and exerting anti-cancer effect. We investigated the effect of aqueous extract of Guem Chung Choon apoptosis in the hippocampus after transient global ischemia using gerbils. Guem Chung Cho is an artificially cultivated Cordyceps, and was supplied from GCordy (Seoul, Korea). Aqueous extract of Guem Chung Cho (50 g) was made by rotary evaporate, and resulting powder 11.5 g was obtained (yield 23 %). Transient global ischemia was induced by ligation of both common carotid arteries for 7 min. Aqueous extract of Guem Chung Cho was administrated orally at 3 respective doses (0.001, 0.01, and 0.1 mg/kg) once a day for 14 consecutive days, beginning 1 day after surgery. Short-term memory was assessed by a step-down avoidance test. Histological study was performed with terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and immunohistochemistry for caspase-3 and 5-bromo-2’-deoxyuridine (BrdU). Western blot for Bcl-2, Bax, brain-derived neurotrophic factor (BDNF), and tyrosine kinase B (TrkB) was conducted. The results revealed that induction of cerebral ischemia impaired short-term memory with increased DNA fragmentation and caspase-3 expression in the hippocampal dentate gyrus. Induction of cerebral ischemia also enhanced expression of pro-apoptotic factor Bax protein and suppressed expression of anti-apoptotic factor Bcl-2 protein in the hippocampus. In addition, cerebral ischemic insult excessively increased cell proliferation in the hippocampal dentate gyrus, whereas, decreased the expressions of BDNF and TrkB in the hippocampus. Guem Chung Cho treatment ameliorated cerebral ischemia-induced impairment of short-term memory. Guem Chung Cho treatment suppressed apoptosis and cell proliferation and enhanced expressions of BDNF and TrkB. These effect of Guem Chung Cho appeared most potently at lowest dosage used in this study, 0.001 mg/kg. We showed that Guem Chung Cho may overcome ischemia-induced apoptotic neuronal cell death, thus facilitates recovery following ischemic cerebral injury. This study was supported by GCordy company.
Kim, Sung-Eun,Ko, Il-Gyu,Hwang, Lakkyong,Choi, In-Young,Shin, Mal-Soon,Kim, Chang-Ju,Kim, Khae-Hawn BioMed Central 2013 Journal of biomedical science Vol.20 No.1
<P><B>Background</B></P><P>Tamsulosin, an α1-adrenoceptor antagonist, and sildenafil, a phosphodiesterase (PDE) inhibitor, are reported to improve lower urinary tract symptoms including overactive bladder (OAB). This study is aimed at investing the effects of tamsulosin and sildenafil and comparing the degree of the suppressive effects on the afferent pathways of micturition between them using an animal model of OAB, the spontaneously hypertensive rat (SHR).</P><P><B>Results</B></P><P>The cystometric parameters, the basal pressure and duration of bladder contraction, were significantly increased in the SHR group as compared with the Wistar-Kyoto (WKY) group. The intercontraction interval also significantly decreased in the SHR group. In the SHR-Tam 0.01 mg/kg group and the SHR-Sil 1 mg/kg group, however, the basal pressure and duration were significantly reduced and the intercontraction interval was significantly prolonged. Moreover, the degree of the expression of c-Fos and NGF was significantly higher in the SHR group as compared with the WKY group. But it was significantly reduced in the SHR-Tam 0.01 mg/kg group and the SHR-Sil 1 mg/kg group. Furthermore, tamsulosin had a higher degree of effect as compared with sildenafil.</P><P><B>Conclusions</B></P><P>In conclusion, α1-adrenergic receptor antagonists and PDE-5 inhibitors may have an effect in improving the voiding functions through an inhibition of the neuronal activity in the afferent pathways of micturition.</P>