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마우스에서 VEGF 발현 Naked DNA 벡터인 pCK-VEGF의 약동력학 및 조직내 분포
도현미(Hyounmie Doh),고준일(Jun-IL Ko),이종진(Jong-Jin Lee),손미원(Miwon Son),조홍찬(Hongchan Cho),김종묵(Jong-Mook Kim ),김병문(Byong-Moon Kim),김선영(Sunyoung Kim) 大韓藥學會 2001 약학회지 Vol.45 No.1
We recently developed a high dfficiency expression vector, pCK, which drives a high level of gane expresion in the skeletal muscles of mice. In this study, we investigated the pharmacokinetics and biodistribution of pCK-VEGF expressing human VEGF165 after intravenous or intramuscular administration. The quantity of pCK-VEGF in the tissues of mice was measured by the PCR method which has a detection limit of approxinately 1 pg of the exogenously added plasmid In the case of intravenous administration, the half life of the pCK-VEGF plasmid in the bloodstream was 1.68 min. After inter-muscular adminstration, the half life of pCK-VEGF plasmid in the bloodstrean was 6.78 min. At 90 min post-administration, 30% of the injected pCK-VEGF was found at the site of injection, where it persisted for up to 8 hours. Less than 1.6% of the injected pCK-VEGF plasmid DNA was detected in highly vascularized tissues such as the lung, kidney, and liver at 90 min post-administration administrated pCK- VEGF presisted for longer periods of time in muscls than in other tissues and that direct intra-muscular injection of pCK-VEGF might be useful for local therapeutic angiogensis.
중증 허혈성 지체질환 환자에서 시행된 vascular endothelial growth factor의 혈관신생 유전자치료 1예
김현중,장신이,김종묵,김선영,김병문,김원배,김덕경 대한내과학회 2003 대한내과학회지 Vol.64 No.1
저자 등은 기존의 치료에 반응하지 않은 중증 허혈성 지체질환 환자를 대상으로 하여 vascular endothelial growth factor를 이용한 혈관신생 유전자 치료를 시행하였다. 치료 후 환자의 허혈에 의한 하지 통증이 현격하게 감소하고 상처의 진행이 측부혈관이 많이 증가됨이 관찰되어 이에 문헌고찰과 함께 보고하는 바이다. We report VEGF-induced angiogenic gene therapy in a patient with critical limb ischemia, who did not respond to conventional treatment. This patient was the first case in a dose-escalating series of phase I clinical trial. The patient had severe resting pain, gangrene and diffuse ulcer in his left foot. Total 1,000㎍ of naked DNA encoding human VEGF165 was administered intramuscularly to 8 sites of the loft lower extremity. Four weeks after the first 1,000㎛ was administered to the same sites (total dose: 2,000㎛). After gene therapy, resting pain gradually reduced and the amount of analgesics taken by the patient decreased. The ischemic wound of lower extremity slightly improved. However, there was no complete wound healing at 12 weeks of treatment. Digital subtraction angiography at 12 weeks after gene therapy showed an increase in collateral vessels at the mid-tibial, ankle and foot arch levels. Immediately and up to 12 weeks, there was no complication related to gene therapy. These findings may be cautiously interpreted to indicate that intramuscular injection of naked plasmid DNA of VEGF_165 may induce therapeutic angiogencsis in a patient with critical limb ischemia. Further clinical evaluation of VEGF-induced gene therapy is needed to evaluate the safety and efficiency of this treatment.(Korean J Med 64:85-90, 2003)