Ischemic stroke and ischemia/reperfusion (I/R) injury induced by thrombolytic therapy are conditions with high mortality and serious long-term physical and cognitive disabilities. They have a major impact on global public health. These disorders are associated with multiple insults to the cerebral microcirculation, including reactive oxygen species (ROS) overproduction, leukocyte adhesion and infiltration, brain blood barrier (BBB) disruption, and capillary hypoperfusion, ultimately resulting in tissue edema, hemorrhage, brain injury and delayed neuron damage. Traditional Chinese medicine (TCM) has been used in China, Korea, Japan and other Asian countries for treatment of a wide range of diseases. In China, the usage of compound TCM preparation to treat cerebrovascular diseases dates back to the Han Dynasty. Even thousands of years earlier, the medical formulary recorded many classical prescriptions for treating cerebral I/R-related diseases. This review summarizes current information and underlying mechanisms regarding the ameliorating effects of compound TCM preparation, Chinese materia medica, and active components on I/R-induced cerebral microcirculatory disturbances, brain injury and neuron damage.
Keywords: 8-OHdG, 8-hydroxydeoxyguanosine; AIF, apoptosis inducing factor; AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; AP-1, activator protein-1; Antioxidant; Asp, aspartate; BBB, brain blood barrier; BMEC, brain microvascular endothelial cell; BNDF, brain-derived neurotrophic factor; Brain blood barrier; CAT, catalase; CBF, cerebral blood flow; COX-2, cyclooxygenase-2; Cav-1, caveolin-1; DHR, dihydrorhodamine 123; DPPH, 1,1-diphenyl-2-picrylhydrazyl radical 2,2-diphenyl-1-(2,4,6-trinitrophenyl) hydrazyl; ERK, extracellular signal-regulated kinase; GABA, γ-aminobutyric acid; GRK2, G protein-coupled receptor kinase 2; GSH, glutathione; GSH-Px, glutathione peroxidase; GSSH, glutathione disulfide; Glu, glutamate; Gly, glysine; HE, hematoxylin and eosin; HIF, hypoxia-inducible factor; HPLC, high performance liquid chromatography; Hyperpermeability; I-κBα, Inhibitory κBα; I/R, ischemia-reperfusion; ICAM-1, intercellular adhesion molecule-1; IL-10, interleukin-10; IL-1β, interleukin-1β; IL-8, interleukin-8; Ischemia/reperfusion; JAM-1, junctional adhesion molecule-1; JNK, Jun N-terminal kinase; LDH, lactate dehydrogenase; Leukocyte adhesion; MAPK, mitogen activated protein kinase; MCAO, middle cerebral artery occlusion; MDA, malondialdehyde; MMPs, matrix metalloproteinases; MPO, myeloperoxidase; MRI, magnetic resonance imaging; NADPH, nicotinamide adenine dinucleotide phosphate; NF-κB, nuclear factor κ-B; NGF, nerve growth factor; NMDA, N-methyl-d-aspartic acid; NO, nitric oxide; NSC, neural stem cells; Neuron; OGD, oxygen-glucose deprivation; PARP, poly-ADP-ribose polymerase; PMN, polymorphonuclear; RANTES, regulated upon activation normal T-cell expressed and secreted; ROS, reactive oxygen species; SFDA, state food and drug administration; SOD, superoxide dismutase; TBARS, thiobarbituric acid reactive substance; TCM, traditional Chinese medicine; TGF-β1, transforming growth factor β1; TIMP-1, tissue inhibitor of metalloproteinase-1; TNF-α, tissue necrosis factor-α; TTC, 2,3,5-triphenyltetrazolium chloride; TUNEL, terminal-deoxynucleoitidyl transferase mediated nick end labeling; Tuj-1, class III β-tublin; VCAM-1, vascular adhesion molecule-1; VEGF, vascular endothelial growth factor; ZO-1, zonula occludens-1; bFGF, basic fibroblast growth factor; cAMP, cyclic adenosine monophosphate; hs-CRP, high-sensitivity C-reactive protein; iNOS, inducible nitric oxide synthase; rtPA, recombinant tissue plasminogen activator.