Zinc(Ⅱ) induced neurological thrombolytic activities have become apparent during thrombolysis process of COVID-19 thrombus prevention, inflammation, fibrin degradation, fibrinolysis of dissolving blood clots, and blood flow reperfusion after thrombolysis. In COVID-19 thrombus prevention, zinc can prevent respiratory thrombosis and pulmonary thromboembolism by inhibition of thrombus formation growth. In COVID-19 inflammation, zinc-induced suppression of inflammation in thrombolysis may be involved that zinc can reduce the inflammation in the abdominal aortic aneurysm (AAA) which zinc has anti-inflammatory and anti-oxidant effects, and immune responses. Fibrin degradation process is involved that zinc binds tissue-type plasminogen activator (tPA), in which atorvastatin decreased cerebral, fibrin, neutrophil, and microvascular platelet deposits. Zn 2+ accelerates fibrin clot formation and increases fiber diameter both in the absence and in presence of coagulation factor (FXIII) and zinc ions effect clot structure of porosity, stiffness, and rheology. In zinc-induced thrombolytic dissolving blood clots, zinc-stabilized t-PA gelatin complex, MMP9 and MMP3 with t-PA are a promising t-PA delivery system, and may facilitate neuroprotection and vital for reperfusion treatment that zinc-induced neurotoxicity has been shown to play a role in neuronal damage and death associated with traumatic brain injury, stroke, seizures, and neurodegenerative diseases with worthing a neuroprotective intervention in stroke. Furthermore, zinc induced ROS in the resolution of a venous thrombus has ROS-mediated cell recruitm and oxidative stress at the site of a venous thrombus and increased ROS production is demonstrated in during ischemia, reperfusion, and restoration of the blood flow.Finally, the zinc(Ⅱ) binding molecular mechanism is considered that Zn 2+ ions may bind to inflammatory, fibrinogen, fibrinolytic, and thrombus proteins respectively by Zn 2+ ions-centered coordinated tetrahedral binding molecular pattern.