Figure 1

Therapeutic targets and mechanisms of brain damage in human and experimental subarachnoid hemorrhage (SAH). Schematic overview of known brain damage mechanisms in humans (left side of the figure) and experimental animals models (right side of the figure). Possible therapeutic options which have been explored in the endovascular puncture model are depicted in light blue. Suggested novel therapeutic options strategies are depicted in green. The red lines depict the target of inhibition. From top to bottom: SAH induces inflammation in the brain reflected by increased expression of adhesion molecules, increased influx of immune cells (depicted are neutrophils, macrophages and T-cells), increased activity of complement system, high mobility group box-1 (HMGB-1) expression, increased expression of transcription factors and cytokine/chemokine production. Different forms of neuronal cell death after SAH are observed; that is, apoptosis, autophagy, necroptosis and necrosis. Lower section: physiological factors in the brain which are altered after SAH. Abbreviations: BIP, Bax-inhibiting peptide; CBF, cerebral blood flow; CPP, cerebral perfusion pressure; EPO, erythropoietin; GA, glycyrrhizic acid; ICP, intracranial pressure; MABP, mean arterial blood pressure; MSCs, mesenchymal stem cells; NBD, NEMO binding domain peptide; Nec-1, necrostatin-1; OPN, osteopontin; PFT, pifithrin.