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배기환,김환묵,이상명 충남대학교 약학대학 의약품개발연구소 1996 藥學論文集 Vol.12 No.-
The cytotoxic effect of Pylorae Herba (pyrola japonica Klenze) against L1210 K-562 cells was studied in vitro. The methanolic extract of Pylorae Radix was added to the culture of L1210 cells and K-562 cells for the cytotoxic activity and the ED50 values of hexane, ethylacetate, buthanol and water fractions from methanolic extract were determined using MTT (3-[4,5-dimethylthiazol-2-yl]-2.5-diphenyltetrazoliumbromide) assay. The active constituent isolated by bioassay guided fractionation followed by purification gave rise to a yellow needle crystal and was clarified to be chimaphilline by the comparison with the published data. The average life spans with it were not prolonged significantly on tumor growth in hybrid female mouse (BDF1-KIST) inoculated subcutaneously with P388 cells.
Pretreatment of Macrophages with Paclitaxel Inhibits iNOS Expression
Mei Hong Li,Jong Soon Kang,Hwanmook Kim,Young Jin Jeon 한국독성학회 2006 Toxicological Research Vol.22 No.2
We demonstrate that paclitaxel, an antitumor agent derived from yew tree, inhibits LPS-induced expression of iNOS gene in RAW 264.7 cells. Previously, paclitaxel has been known to induce iNOS gene expression in macrophages. However, in this report we described that the pretreatment of macrophages with paclitaxel (0.1 μM) for 8 h inhibited LPS-induced iNOS gene expression. Pretreatment of RAW 264.7 cells with paclitaxel significantly inhibited LPS-stimulated nitric oxide (NO) production. Western immunoblot of iNOS and RT-PCR analysis showed that the decrease of NO was due to the inhibition of iNOS gene expression in RAW 264.7 cells. Immunocytochemical staining of iNOS further confirmed that pretreatment of macrophages with paclitaxel inhibited macrophage activation. Electrophoretic mobility shift assay showed that paclitaxel inhibited NF-κ/Rel DNA binding. Collectively, these series of experiments indicate that paclitaxel inhibits iNOS gene expression by blocking NF-κB/Rel activation.
CD18 단일클론항체와 Superoxide Dismutase을 이용한 재관류 손상의 예방
강낙헌,손경동,한기택,임풍,김환묵 大韓成形外科學會 1998 Archives of Plastic Surgery Vol.25 No.1
Prolonged ischemia results in cellular necrosis and only prompt restoration of blood flow will prevent this type of injury. However, reperfusion itself can cause significant injury of previously ischemic tissue, i.e. "reperfusion injury'. This is an issue of concern in many areas of reconstructive surgery including free tissue transfer and replantation. Many factors have been implicated in the cause of reperfusion injury. Oxygen free radicals have enjoyed increasing popularity recently, but leukocytes had been thought to have a role only in the healing process that follows ischemic injury. Current studies in myocardium, liver and intestine have shown a dramatic increase in tissue leukocytes after ischemia-reperfusion and evidence implicating leukocytes in pathogenesis of ischemia-reperfusion injury has come from studies demonstrating significant injury reduction by depletion of circulating neutrophils. Therefore, increased neutrophil adhesiveness is a critical early step in the sequence of events leading to neutrophil-mediated injury. The purpose of this study is to evaluate the effect of CDl8 monoclonal antibody(CDl8 mAb), blocking antibody of neutrophil adherence, and superoxide dismutase (SOD), free radical scavenger, on reperfusion injury in rat epigastric island skin flap. The epigastric pedicle was occluded for six hours with ambient temperature at 22±1℃. The epigastric nerve was carefully dissected out and left intact to minimize autocannibalization. The flaps were sutured back down to their beds over interposed silicone sheets to prevent plasmatic imbibition. Fifteen minutes before reperfusion, the flaps were perfused with saline, CDl8 mAb(1 mg/kg), SOD(20,000 unit/kg) or CDl8 mAh/SOD(1 mg/kg + 20,000unit/kg). Percentage of flap survival was assessed by computerized planimetry on the seventh day. Tissue biopsies for myeloperoxidase(MPO) and malonyldialdehyde (MDA) were obtained at 24 hours after reperfusion. The results were as follows. 1. Percentage of flap survival was significantly increased in CDl8 mAb/SOD, CDl8 mAb and SOD groups in order, compared to the control(P < 0.05). Percentage of flap survival was significantly increased in CDl8 mAb group as compared with SOD group(p < 0.05). Percentage of flap survival significantly increased in CDl8 mAb/SOD group as compared with CDl8 mAb and SOD groups(p < 0.05) 2. MPO activity was significantly decreased in CDl8 mAb/SOD, CDl8 mAb and SOD groups(p < 0.01). MPO activity was significantly decreased in CDl8 mAb group as compared with SOD group. (p < 0.01). 3. MDA content was significantly decreased in CDl8 mAb/SOD, CDl8 mAb and SOD groups (p < 0.01), but the difference between CDl8 mAb and SOD groups was not significant. From those above results, we get to the conclusion that blocking neutrophil adherence and/or aggregation with monoclonal antibodies to CDl8 as compared with radical scavenger significantly ameliorates reperfusion injury. It is suggested that combination of modalities with antiadhesion therapy and radical scavenger may have a synergistic effect of improving flap survival and may be the optimal prevention of ischemiareperfusion injury.