Plasmin is generally known as a promotor of
inflammation. Recent advancement suggests that it has a complex role as immunity modulator. Pharmacological inhibition of
plasmin production and activity has been proven to improve neurological outcomes in
traumatic brain injury and
subarachnoid hemorrhage, most probably by preventing re-
bleeding. The immune-modulatory properties of
antifibrinolytics, however, suggest that they probably have effects unrelated to fibrinolysis inhibition, which are currently not adequately harnessed. The present work aims to give an account of the existing data regarding
antifibrinolytics as agents influencing
neuroinflammation. Preclinical and clinical studies on the possible influence of
antifibrinolytics on
neuroinflammation are scarce. However, the emerging evidence suggests that inhibition of
plasmin(
ogen) activity can ameliorate
neuroinflammation to some extent. This data demonstrate that
plasmin(
ogen) is not exclusively involved in fibrinolysis, but also has other substrates and can precipitate in inflammatory processes. Investigation on the role of
plasmin as the factor for the development of
neuroinflammation shows the significant potential of
antifibrinolytics as
pharmacotherapy of neuroinflammationm, which is worthy of further exploration.