Background: Stroke is one of the largest problems and clinical-social challenges within neurology and, in general, pathology. Here, we briefly reviewed the main pathophysiological mechanisms of ischemic stroke, which represent targets for medical interventions, including for a calf blood deproteinized hemodialysate/ultrafiltrate.
Methods: We conducted a systematic review of current related literature concerning the effects of Actovegin®, of mainly the pleiotropic type, applied to the injury pathways of ischemic stroke.
Results: The bibliographic resources regarding the use of Actovegin® in ischemic stroke are scarce. The main Actovegin® actions refer to the ischemic stroke lesion items' ensemble, targeting tissue oxidation, energy metabolism, and glucose availability through their augmentation, combating ischemic processes and oxidative stress, and decreasing inflammation (including with modulatory connotations, by the nuclear factor-κB pathway) and apoptosis-like processes, counteracting them by mitigating the caspase-3 activation induced by amyloid β-peptides.
Conclusion: Since no available therapeutic agents are capable of curing the central nervous system's lesions, any contribution, such as that of Actovegin® (with consideration of a positive balance between benefits and risks), is worthy of further study and periodic reappraisal, including investigation into further connected aspects.
Keywords: Actovegin®; deproteinized ultrafiltrate/hemodialysate compound; endogenous defense activity; ischemic stroke; pathophysiological/damage mechanisms; pleiotropic action.