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Effects of Tetramethylpyrazine on Functional Recovery and Neuronal Dendritic Plasticity after Experimental Stroke.

Lin JB, Zheng CJ, Zhang X, Chen J, Liao WJ, Wan Q - Evid Based Complement Alternat Med (2015)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Rehabilitation Medicine, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.

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.

No MeSH data available.


Related in: MedlinePlus

The structure of TMP.
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fig1: The structure of TMP.

Mentions: 2,3,5,6-Tetramethylpyrazine (TMP, Figure 1) is an active ingredient extracted from a traditional Chinese herbal medicine Ligusticum chuanxiong Hort. and has been widely used in ischemic stroke by Chinese doctors [4]. TMP exerts pharmacological effects in multiple ways with multiple targets. 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 [5–7]. Besides the above-mentioned effects, it is also 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. Recently, it has been found that TMP could protect hepatic fibrosis by modulating multiple signal pathways [9–11]. Furthermore, TMP had a significant therapeutic effect on diabetic nephropathy [12], which could be mediated by downregulated expression of vascular endothelial growth factor in the kidney and reduction of lipoperoxidation [13, 14]. Additionally, TMP has been reported to have beneficial effects in various types of cancer [15–17]. 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], thrombolytic effect [22], enhancing neurogenesis, and cell differentiation [23].


Effects of Tetramethylpyrazine on Functional Recovery and Neuronal Dendritic Plasticity after Experimental Stroke.

Lin JB, Zheng CJ, Zhang X, Chen J, Liao WJ, Wan Q - Evid Based Complement Alternat Med (2015)

The structure of TMP.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4563062&req=5

fig1: The structure of TMP.
Mentions: 2,3,5,6-Tetramethylpyrazine (TMP, Figure 1) is an active ingredient extracted from a traditional Chinese herbal medicine Ligusticum chuanxiong Hort. and has been widely used in ischemic stroke by Chinese doctors [4]. TMP exerts pharmacological effects in multiple ways with multiple targets. 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 [5–7]. Besides the above-mentioned effects, it is also 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. Recently, it has been found that TMP could protect hepatic fibrosis by modulating multiple signal pathways [9–11]. Furthermore, TMP had a significant therapeutic effect on diabetic nephropathy [12], which could be mediated by downregulated expression of vascular endothelial growth factor in the kidney and reduction of lipoperoxidation [13, 14]. Additionally, TMP has been reported to have beneficial effects in various types of cancer [15–17]. 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], thrombolytic effect [22], enhancing neurogenesis, and cell differentiation [23].

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Rehabilitation Medicine, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.

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.

No MeSH data available.


Related in: MedlinePlus