Current Synthesis and Systematic Review of Main Effects of Calf Blood Deproteinized Medicine (Actovegin ® ) in Ischemic Stroke

• Published in: International journal of molecular sciences Vol. 21; no. 9; p. 3181
• Main Authors: Firan, Florentina Carmen, Romila, Aurelia, Onose, Gelu
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 30.04.2020; MDPI
• Subjects: Actovegin; Amyloid beta-Peptides - pharmacology; Animals; Antioxidants - therapeutic use; Apoptosis; Blood; Brain Ischemia - drug therapy; Brain Ischemia - metabolism; Caspase-3; Cell adhesion & migration; Central nervous system; Chemical compounds; Curing agents; Cytokines; deproteinized ultrafiltrate/hemodialysate compound; Disability; endogenous defense activity; Energy metabolism; Gene expression; Glucose metabolism; Heme - analogs & derivatives; Heme - therapeutic use; Hemodialysis; Humans; Hypoxia; Injuries; Ischemia; ischemic stroke; Literature reviews; Mortality; Nervous system; Neurology; Oxidation; Oxidative stress; pathophysiological/damage mechanisms; Peptides; Pharmacology; pleiotropic action; Review; Stroke; Stroke - drug therapy; Stroke - metabolism; pleiotropic action; deproteinized ultrafiltrate/hemodialysate compound; pathophysiological/damage mechanisms; endogenous defense activity; ischemic stroke; Actovegin
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms21093181

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. 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. 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. 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.