Nattokinase Reduces Brain Infarction and Coagulation Parameters in Gerbil Cerebral Ischemia-Reperfusion

This animal study evaluated the neuroprotective and fibrinolytic effects of oral nattokinase pretreatment in 42 gerbils subjected to focal cerebral ischemia-reperfusion, measuring brain infarct volume and coagulation parameters.

Nattokinase pretreatment significantly reduced brain infarct volume by 54–68% in a dose-dependent manner. Coagulation parameters — including fibrinogen and activated partial thromboplastin time (APTT) — were normalized toward baseline by low-dose nattokinase, while prothrombin time remained unchanged.

The finding of brain infarct volume reduction in a gerbil ischemia model is mechanistically interesting but faces significant translational barriers to human cerebrovascular or coronary artery disease applications. The gerbil ischemia model uses carotid clamping to induce focal ischemia — a different mechanism from the spontaneous plaque rupture and thrombosis that causes most human strokes and MIs.

The fundamental question for any nattokinase study remains pharmacokinetic: whether enzymatically active nattokinase reaches systemic circulation after oral ingestion, and at what concentrations. Animal studies do not resolve this question because they use routes of administration, doses, and animal pharmacokinetics that do not map reliably to human oral dosing.

There is no randomized clinical trial evidence that oral nattokinase supplementation reduces cerebrovascular or coronary events in humans.

We rate the evidence limited. A gerbil model study showing that nattokinase reduces brain infarct volume in experimental ischemia — mechanistically interesting basic science that faces substantial translational barriers to human clinical application.