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성연희(Yeon Hee Seong),강종구(Jong Koo Kang),안희열(Hee Yul Ahn),김선돈(Sun Don KIm),이선애(Sun Ae Lee),조순옥(Soon Ok Jo),유보림(Bo Rim Yoo),정영신(Young Shin Jung),홍은경(Eun Kyung Hong),한영복(Young Bok Han) 한국응용약물학회 1997 Biomolecules & Therapeutics(구 응용약물학회지) Vol.5 No.4
General pharmacological properties of AG 60 (mixture of acriflavine and guanosine (1:1, w/w)), which has anticancer effect, following intramuscular administration were examined in terms of effects on central nervous system, gastrointestinal system, cardiovascular system, respiratory system and autonomic nervous system in mice, rats, guinea-pigs and rabbits. AG 60 at the dose of 15 mg/kg had no influences on pentobarbital sleeping time, spontaneous motor activity, chemoshock produced by pentylenetetrazole solution, writhing syndromes induced by 0.8% acetic acid solution, and motor coordination of mice. However, AG 60 at the dose of 7.5 and 15 mg/kg caused significant decrease of normal body temperature 1 and/or 2 h after the administration. No influence on body temperature was observed at 3.75 mg/kg in mice. Gastric secretion of rat and intestinal motility of mice were not influenced by the dose of 15 mg/kg. In terms of autonomic nervous system, AG 60 did not show direct effect and inhibitory or augmentative action of histamine- or acetylcholine-induced contractions at the concentration of 5 mg/L in the isolated ileum of guinea-pig. The administration of 15 mg/kg of AG 60 did not affect mean arterial blood pressure and heart rate in rat. AG 60 (15 mg/kg) given to anesthetized rabbits showed no effect on respiratory rate.
Urinary Trypsin Inhibitor ( UTI ) 의 일반약리작용
성연희(Yeon Hee Seong),조순옥(Sun Ok Jo),이선애(Seon Ae Lee),임화경(Hwa Kyung Lim),장춘곤(Choon Gon Jang),김학성(Hack Seang Kim),강종구(Jong Koo Kang) 한국응용약물학회 1996 Biomolecules & Therapeutics(구 응용약물학회지) Vol.4 No.4
General pharmacological properties of urinary trypsin inhibitor (UTI) following intravenous administration of 1,000,000 units/㎏ were examined in terms of effects on central nervous system, cardiovascular system, respiratory system, gastrointestinal system in mice, rats and rabbits. Administration of UTI (1,000,000 units/㎏, iv) had no effect on central nervous system; no influences on pentobarbital sleeping time, spontaneous activity, normal body temperature, chemoshock produced by pentylenetetrazole solution, writhing syndromes induced by 0.6% acetic acid solution, and motor coordination of mice. The administration of UTI (1,000,000 units/㎏, iv) in rats had no effect on systolic blood pressure and pulse rate. UTI (500,000 units/㎏, iv) given to anesthetized rabbits showed no effect on respiratory rate. However, it showed significant elevation of respiratory rate at the concentration of 1,000,000 units/㎏. Gastric secretion of rat and intestinal motility of mice were not influenced by the dose of 1,000,000 units/㎏. In terms of autonomic nervous system, the material did not show direct effect and inhibitory or augmentative action of histamine- or acetylcholine-induced contraction at the concentration of 2,000 units/ml in the isolated ileum of guinea pig.
김주연,주현수,반주연,송경식,성연희,Kim, Joo-Youn,Ju, Hyun-Soo,Ban, Ju-Yeon,Song, Kyung-Sik,Seong, Yeon-Hee The Korean Society of Medicinal Crop Science 2008 한국약용작물학회지 Vol.16 No.6
Moutan cortex, the root bark of Paeonia suffruticosa Andrews (Paeoniaceae), has pharmacological effects such as anti-inflammatory, antiallergic, analgesic and antioxidant activities. We investigated a methanol extract of Moutan cortex for neuroprotective effects on neurotoxicity induced by amyloid ${\beta}$ protein ($A{\beta}$) (25-35) in cultured rat cortical neurons. Exposure of cultured cortical neurons to $10\;{\mu}M\;A{\beta}$ (25-35) for 24 h induced neuronal apoptotic death. Moutan cortex inhibited $10\;{\mu}M\;A{\beta}$ (25-35)-induced neuronal cell death at 30 and $50\;{\mu}g/m{\ell}$, which was measured by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. Moutan cortex inhibited $10\;{\mu}M\;A{\beta}$ (25-35)-induced elevation of intracellular calcium concentration ($[Ca^{2+}]_i$), and generation of reactive oxygen species (ROS) which were measured by fluorescent dyes. Moutan cortex also inhibited glutamate release into medium induced by $10\;{\mu}M\;A{\beta}$ (25-35), which was measured by HPLC. These results suggest that Moutan cortex prevents $A{\beta}$ (25-35)-induced neuronal cell damage by interfering with the increase of $[Ca^{2+}]_i$, and then inhibiting glutamate release and ROS generation. Moutan cortex may have a therapeutic role in preventing the progression of Alzheimer's disease.