Abstract
The 2,3,5,6-tetramethylpyrazine (TMP) has been widely used in the treatment of ischemic stroke by Chinese doctors. Here, we report the effects of TMP on functional recovery and dendritic plasticity after ischemic stroke. A classical model of middle cerebral artery occlusion (MCAO) was established in this study. The rats were assigned into 3 groups: sham group (sham operated rats treated with saline), model group (MCAO rats treated with saline) and TMP group (MCAO rats treated with 20 mg/kg/d TMP). The neurological function test of animals was evaluated using the modified neurological severity score (mNSS) at 3 d, 7 d, and 14 d after MCAO. Animals were euthanized for immunohistochemical labeling to measure MAP-2 levels in the peri-infarct area. Golgi-Cox staining was performed to test effect of TMP on dendritic plasticity at 14 d after MCAO. TMP significantly improved neurological function at 7 d and 14 d after ischemia, increased MAP-2 level at 14 d after ischemia, and enhanced spine density of basilar dendrites. TMP failed to affect the spine density of apical dendrites and the total dendritic length. Data analyses indicate that there was significant negative correlation between mNSS and plasticity measured at 14 d after MCAO. Thus, enhanced dendritic plasticity contributes to TMP-elicited functional recovery after ischemic stroke.
Highlights
Stroke is the leading cause of long-term disability in the western world, which is a severe disease characterized by its high morbidity, mortality, disability, and recurrence [1]
The animals were randomly assigned into 3 groups: sham group, model group (MCAO rats treated with saline), and TMP group (MCAO rats treated with 20 mg/kg/d TMP (Aladdin Chemistry Co., Ltd., Shanghai, China))
In sham group, MAP-2(+) cells showed staining mainly in the dendrites of the cells; in ischemic animals, we examined the expression of MAP-2 in periinfarct area at 3 d, 7 d, and 14 d after middle cerebral artery occlusion (MCAO); the level of MAP-2 markedly decreased compared to sham group and persistently increased from 3 d to 14 d after stroke, which was consistent with previous study [48]
Summary
Stroke is the leading cause of long-term disability in the western world, which is a severe disease characterized by its high morbidity, mortality, disability, and recurrence [1]. TMP is reported to protect ischemia reperfusion injury of heart, brain, and kidney via reducing oxidative stress, attenuating Ca2+ overload, inhibiting apoptosis, inhibiting inflammatory reaction, and so forth [5,6,7]. It is demonstrated that TMP can inhibit platelet aggregation, depress blood viscosity, and ameliorate microcirculation [8], which could be another important mechanism to treat cardiovascular and cerebrovascular diseases. Specific to ischemic stroke, according to previous studies, TMP can play a protective role through the following mechanisms: antiexcitotoxicity [18], inhibiting inflammatory reaction [19], anti-apoptosis [20], antioxidant activity [21], suppression of calcium [21], Evidence-Based Complementary and Alternative Medicine
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