The human plasma lipoprotein-associated phospholipase A2 (Lp-PLA2) is secreted, by the mature macrophages and lymphocytes, which predominantly binds to low-density lipoprotein. Studies in recent years have demonstrated that Lp-PLA2 plays an important role in the process of atherogenesis. Its gene polymorphisms are associated with the occurrence of ischemic stroke, and its specific inhibitor has anti-atherogenic effects. Lp-PLA2 may be a novel independent risk factor and a therapeutic target for ischemic stroke.

Protein Z (PZ) is a vitamin K-dependent protein. As a cofactor for the protein Z-dependent protease inhibitor (ZPI), it inhibits coagulation factor X under the existence of phospholipid and calcium ion, and increases the ZPI activity by nearly 1000-fold, thus it plays a role in the process of thrombosis. ZPI inhibits coagulation factor Ⅺ a alone. ZPI activity is also consumed in the process of inhabiting factor Ⅹa and Ⅺa. This article reviews the biological characteristics of PZ and ZPI and their association with stroke.

Control of hypertension is essential for stroke prevention. For most patients, the monotherapy often fails to lower blood pressure to normal levels, while the combination therapy can increase the effect of lowering blood pressure, however, not all the antihypertensive drugs have good efficacy. The early data analysis of the Chinese Hypertension Intervention Efficacy Study and the subgroup analysis of the KYOTO HEART study have showed that dihydropyridine calcium channel blocker amlodipine and angiotensin receptor blocker valsartan are both the most effective antihypertensive drugs in the prevention of stroke.

Aquaporin-4 (AQP4) is an important structural basis for water regulation and trans- portation in the central nervous system,which participates in physiopathological processes, such as cerebrospinal fluid reabsorption, osmotic regulation, and cerebral edema formation. Protein kinase C (PKC) exists in various cells, it catalyzes the phosphorylation of serine or threonine residues on various protein substrates.In recent years, studies have found that there is a certain correlation between the expressions of AQP4 and PKC after ischemic stroke.This article re- views the distribution,function,functional regulation of AQP4 and PKC,and their relations in ischemia-reperfusion.

Cerebral artery atherosclerosis is the main reason leading to cerebral infarction. CD40/CD40L overexpression will stimulate the immune and inflammatory responses,leading to local inflammatory cell infiltration within the atherosclerotic plaque, triggering plaque rupture, and thus causing cerebral infarction. Studies have suggested that that CD40L is associated with the severity of cerebral infarction, Therefore, clinical detection of CD40L can be used as an indicator for identifying the severity of cerebral infarction to guide clinical treatment.

In addition to lipid-lowering,statins also have a wide range of pleiotropy.This article synthesizes and induces the pleiotropy of statins in the prevention and treatment of ischemic cerebrovascular diseases.

Stroke canlead to hemiplegia,aphasia,and cognitive impairment,and also complicate with seizure and epilepsy.In recent years,there are more and more studies about post-stroke seizure and post-stroke epilepsy,but the main focus is on risk factors.This article reviews the risk factors,pathogenesis,and treatment of post-stroke seizure and post-stroke epilepsy.

Neurotrophic factors binds with their specific receptors tropomyosin-related kinase (Trk)to protect ischemic neurons during ischemic brain injury.The studies of the activation mode of Trk expression and its relationship with cerebral ischemia have important value.This article reviews the biological characteristics and action pathway of Trk,its relationship with cerebral ischemia,and its application prospect.

Angiotensin Ⅱ receptor blockers(ARBs)decrease blood pressure,reverse vascular remodeling,and activate angiotensinⅡsubtype 2(AT2)receptors in order to improve the levels of angiotensinⅡ(AngⅡ),dilate blood vessels,protect against proliferation,and regulate lipid by blocking angiotcnsinⅡtype 1(AT1)receptors.Further understanding the action mech-anism of ARB in neuroprotection may provide a new idea for the treatment of ischemic stroke in clinical practice.

Objective To investigate the expression of IGF-1 in cerebral tisse,and its correlation with Glutamate expression and neuronal apoptosis,and to study the role of IGF-1 in the pathophysiologie process of ICH.Methods ICH model was induced in rats by infusing 50?l autologous blood into the eaudate nucleus with stereotaetie device.The animals were randomly divided into sham-operation group,ICH group and exogenous IGF-1 intervention group.Every rat was killed and brain tissue was collected.Immunohistoehemitry assay was used to detect the expression of IGF-1 and Glutamate,and TUNEL method used to detect apoptosis in cerebral tissues.Result At 2 hours after ICH,IGF-1 positive cells appeared around the hematoma in the brain,peaked after 24 hours,and returned to normal level on the 7th day. Glutamate positive cells appeared around the hematoma at 2 hours,peaked on the 3rd day,and its high level expression lasted to the 7th day.TUNEL- positive cells appeared at 8 hours,peaked on the 3rd day,and few apoptotic ceils could be found on the 7th day.The expression of IGF-1 was positively correlated with apoptotie cells and the expression of Glutamate.The amounts of Glutamate positive cells and TUNEL positive cells were significantly reduced after intervention with exogenous IGF-1.Conclusion IGF-1 participated in the pathophysiologic course of ICH.IGF-1 repaired and protected the brain tissue from damage after ICH.