image: At 1.5 hours after thrombolysis, the anterior and middle cerebral arteries were recanalized in dogs with acute cerebral embolism. view more
Credit: <i>Neural Regeneration Research</i>
Among the drugs used for acute ischemic stroke, recombinant tissue plasminogen activator is widely accepted internationally. In China, urokinase has been widely used for thrombolysis after acute ischemic stroke. Pro-urokinase is the precursor of urokinase. Compared with urokinase, pro-urokinase has greater ability to dissolve thrombus and is safer to use. However, most countries do not recognize urokinase for thrombolytic treatment after acute ischemic stroke, which has not been approved for clinical use. Dr. Wenli Hu and team from Beijing Chao-Yang Hospital, Capital Medical University in China compared the thrombolytic effects of pro-urokinase, recombinant tissue plasminogen activator, and urokinase in a dog model of acute cerebral embolism. They found that jematoxylin and eosin staining showed no hematoma in the infarcted area after thrombolysis with any of the three therapies, and neuronal apoptosis after cerebral infarction was also not attenuated. The results of angiography showed that recanalization after thromboembolism was similar after thrombolysis with pro-urokinase and recombinant tissue plasminogen activator, and that both these drugs were more effective than urokinase. The relevant article was published in the Neural Regeneration Research (Vol. 9, No. 5, 2014).
Article: " Pro-urokinase promotes angiogenesis but does not reduce neuronal apoptosis in infarcted cerebral tissue," by Wei Qin1, Lei Yang1, Hongmei Guo2, Ning Xiang3, Wenli Hu1 (1 Department of Neurology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China; 2 Department of Neurology, Affiliated Tangshan Workers' Hospital of Hebei Medical University, Tangshan, Hebei Province, China; 3 Department of Neurology, People's Hospital of Qinhuangdao, Qinhuangdao, Hebei Province, China)
Qin W, Yang L, Guo HM, Xiang N, Hu WL. Pro-urokinase promotes angiogenesis but does not reduce neuronal apoptosis in infarcted cerebral tissue. Neural Regen Res. 2014;9(5):502-503.
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