Background and Purpose: The mechanism of action of
Batroxobin included the decomposition of the
fibrinogen to
fibrin degradation products (FDPs) and
D-dimer and mobilization of endothelial cells to release endogenous nt-PA and to promote thrombolysis. This review aims to summarize current study findings about
batroxobin on correcting cerebral arterial, venous, and
peripheral vascular diseases, to explore the mechanism of
batroxobin on anti-
thrombosis process. Methods: A thorough literature search was conducted utilizing the PubMed Central (PMC) and EMBASE databases to identify studies up to June 2021. Data from clinical studies and animal experiments about
batroxobin were extracted, integrated and analyzed based on Cochrane handbook for systematic reviews of interventions approach and the Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols (
PRISMA-P), including the condition of subjects, the usage and dosage, research observation index and main findings. Results: A total of 62 studies were enrolled in this systematic review, including 26 clinical studies and 36 animal experiments. The 26 clinical studies involved 873 patients with arterial ischemic events, 92 cases with cerebral
venous thrombosis, 13 cases with cerebral cortical vein
thrombosis, and 1,049 cases with
peripheral vascular diseases. These patients included 452 males and 392 females aged 65.6 ± 5.53 years. The results revealed that
batroxobin had broad effects, including improving clinical prognosis (n = 12), preventing
thrombosis (n = 7), promoting thrombolysis (n = 6), and improving vascular
cognitive dysfunction (n = 1). The effects of
batroxobin on reducing neuronal apoptosis (n = 8),relieving cellular
edema (n = 4), improving spatial memory (n = 3), and promoting thrombolysis (n = 13) were concluded in animal experiments. The predominant mechanisms explored in animal experiments involved promoting depolymerization of
fibrinogen polymers (n = 6), regulating the expression of related molecules (n = 9); such as
intercellular adhesion molecule,
heat shock proteins,
tumor necrosis factor), reducing oxidative stress (n = 5), and reducing
inflammation response (n = 4). Conclusion:
Batroxobin can correct both arterial and venous ischemic diseases by promoting depolymerization of
fibrinogen polymers, regulating the expression of related molecules, reducing oxidative stress, and reducing the
inflammation response.