Thrombolytic activity of cheonggukjang kinase in recovery from brain damage in a rat cerebral embolic stroke model

作     者：Angella M Anthony Jalin Chae Kwan Lee Chae Yeon Lee A Reum Kang Chung Mu Park Jae Ho Cha Jeong Hwan Kim Soo Woong Lee Young Sun Song Jong Tae Lee Sung Goo Kang 

作者机构：School of Biological SciencesFirst Research GroupInje University Institute of Environmental and Occupational Medicine & Department of Occupational and Environmental MedicinePusan Paik HospitalInje University Department of Smart Foods & DrugsInje University Department of MicrobiologyPusan National University Division of Applied Life ScienceGyeongsang National University Advanced Research Center for Multiple MyelomaDepartment of MicrobiologyBio-Marker Research Center for Personalized TherapyCollege of MedicineInje University 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2010年第5卷第24期

页      面：1875-1882页

核心收录：

学科分类：1008[医学-中药学(可授医学、理学学位)] 1006[医学-中西医结合] 100602[医学-中西医结合临床] 10[医学] 

基　　金：the National Research Foundation of Korea,funded by the Korean Ministry of Education,Sci-ence and Technology,No.2007-0055330 Inje Univer-sity Research Grant (2008) 

主　　题：brain damage cheonggukjang kinase fibrin clot lysis assay middle cerebral artery occlusion platelet rich clot lysis assay thrombolytic activity 

摘      要：Cheonggukjang is a soybean paste made by fermenting whole cooked soybeans with Bacillus subtilis. Cheonggukjang contains a fibrinolytic enzyme that could provide clinical applications for removing blood clots. In the present study, the term ＂cheonggukjang kinase＂ （CGK） was used to refer to this fibrinolytic enzyme. The thrombolytic effects of CGK were analyzed in a rat model of cerebral embolic stroke produced by middle cerebral artery occlusion （MCAO）. Results from fibrin and platelet-rich clot lysis assays demonstrated that thrombolytic activity was greatest in CGKs, which were cultured for 40 hours. In addition, T50, the time needed to decompose 50% of the clot, did not change with plasminogen treatment, indicating that CGK was not a plasminogen activator, but was rather presumed to act as a plasmin-like protein. An intravenous infusion of CGK （1 U plasmin-like activity/100 μg CGK/kg） at 1 hour after MCAO resulted in removal of clots in a rat model of cerebral embolic stroke. CGK-treated groups exhibited a significant dose-dependent reduction in infarct volume. CGK treatment also improved functional recovery, as assessed by neurological deficit scores. Decreased infarct volume and improved functional recovery following CGK treatment was greater compared with recombinant tissue plasminogen activator （10 mg/kg）. These results suggested that CGK effectively reduced infarct volume and improved functional recovery following ischemic brain injury. CGK exhibits a number of potential clinical applications ir the treatment of cerebral embolic stroke.