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SD계 흰쥐에서 마황 추출물의 아급성 경구 독성 시험 연구
최동기 ( Dong Gi Choi ),심경준 ( Kyung Jun Shim ),최봉재 ( Bong Jae Choi ),박수연 ( Soo Yeon Park ),장문석 ( Mun Seog Chang ),박성규 ( Seong Kyu Park ) 대한본초학회 2008 大韓本草學會誌 Vol.23 No.4
Objectives: Ephedrae herba, also known as Ma-huang, is a traditional Korean medicinal herb. It has been used to treat asthma, nose and lung congestion, and fever with anhidrosis for centuries. Recently, Ma-huang was used as a source of ephedrine in many dietary supplements for weight reduction in the United States. The objective of this study was to investigate the subacute toxicity of ephedrae herba extract in rats. Methods: SPF Sprague-Dawley male rats were administered orally with ephedrae herba extract for 4 weeks as several doses(0, 125, 250, 500, 1,000, and 2,000 mg/kg). We examined number of deaths, clinical signs, body weights and gross findings for experimental period. Results: No dead animals were found during the experimental period. In addition, no differences were found between control and treated groups in clinical signs, hematology, serum biochemistry, and other findings. Conclusions: In conclusion, above data suggest that no observed adverse effect level of ephedrae herba extract in SD rats might he over 2,000 mg/kg/day in this study.
이시영,최동기,곽아름,김시내,Tam Thanh Nguyen,길가애,김은혜,유광하,김인애,이영민,전현정,Edward D. Chan,Xiyuan Bai,김현우,김용성,김수현 대한면역학회 2017 Immune Network Vol.17 No.2
The induction of interleukin (IL)-32 in bone marrow (BM) inflammation is crucial in graft versus host disease (GvHD) that is a common side effect of allogeneic BM transplantation. Clinical trials on a-1 antitrypsin (AAT) in patients with GvHD are based on the preliminary human and mouse studies on AAT reducing the severity of GvHD. Proteinase 3 (PR3) is an IL-32-binding protein that was isolated from human urine. IL-32 primarily induces inflammatory cytokines in myeloid cells, probably due to PR3 expression on the membrane of the myeloid lineage cells. The inhibitory activity of AAT on serine proteinases may explain the anti-inflammatory effect of AAT on GvHD. However, the anti-inflammatory activity of AAT on BM cells remains unclear. Mouse BM cells were treated with IL-32g and different inflammatory stimuli to investigate the anti-inflammatory activity of AAT. Recombinant AATFc fusion protein inhibited IL-32g-induced IL-6 expression in BM cells, but failed to suppress that induced by other stimuli. In addition, the binding of IL-32g to PR3 was abrogated by AAT-Fc. The data suggest that the specific antiinflammatory effect of AAT in mouse BM cells is due to the blocking of IL-32 binding to membrane PR3.