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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 expression levels of MAP-2 within peri-infarct area of three groups in sham, model, and TMP groups at 3 d, 7 d, and 14 d after MCAO. (a) Immunohistochemical staining of three groups (400x). (b) MAP-2 levels of three groups through measuring the integral optical density (IOD). Data were presented as mean ± standard deviation (n = 6). *P < 0.01 and **P < 0.001.
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fig6: The expression levels of MAP-2 within peri-infarct area of three groups in sham, model, and TMP groups at 3 d, 7 d, and 14 d after MCAO. (a) Immunohistochemical staining of three groups (400x). (b) MAP-2 levels of three groups through measuring the integral optical density (IOD). Data were presented as mean ± standard deviation (n = 6). *P < 0.01 and **P < 0.001.

Mentions: In this study, IOD values were applied to indicate the expression of MAP-2 (Figure 6). In sham group, obvious MAP-2 immunostaining was observed in the dendrites of the cells. Repeated measures analysis of variance showed there was significant group effects (F = 77.753, P < 0.001). Post hoc analyses showed that there were significant differences between three groups at 3 d (sham: 38635.39 ± 2649.21 versus model: 17958.93 ± 1244.88 versus TMP: 19128.20 ± 1795.69; F = 205.913, P < 0.001), 7 d (sham: 38009.15 ± 2715.61 versus model: 22635.95 ± 2102.93 versus TMP: 25521.22 ± 1764.14; F = 80.61, P < 0.001), and 14 d (sham: 39059.86 ± 2831.29 versus model: 31203.85 ± 2478.53 versus TMP: 37147.30 ± 2168.38; F = 16.017, P < 0.001). Compared to sham group, rats in model group showed significantly lower expression of MAP-2 (3 d, 7 d, and 14 d all P < 0.001; decreased 53.52%, 40.45%, and 20.11%, resp.), although they exhibited an increasing trend from 3 d to 14 d after MCAO. TMP treatment resulted in upregulation in MAP-2 expression in peri-infarct area compared to model group at 14 d (P = 0.003; increased 19.05%) after MCAO.


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 expression levels of MAP-2 within peri-infarct area of three groups in sham, model, and TMP groups at 3 d, 7 d, and 14 d after MCAO. (a) Immunohistochemical staining of three groups (400x). (b) MAP-2 levels of three groups through measuring the integral optical density (IOD). Data were presented as mean ± standard deviation (n = 6). *P < 0.01 and **P < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4563062&req=5

fig6: The expression levels of MAP-2 within peri-infarct area of three groups in sham, model, and TMP groups at 3 d, 7 d, and 14 d after MCAO. (a) Immunohistochemical staining of three groups (400x). (b) MAP-2 levels of three groups through measuring the integral optical density (IOD). Data were presented as mean ± standard deviation (n = 6). *P < 0.01 and **P < 0.001.
Mentions: In this study, IOD values were applied to indicate the expression of MAP-2 (Figure 6). In sham group, obvious MAP-2 immunostaining was observed in the dendrites of the cells. Repeated measures analysis of variance showed there was significant group effects (F = 77.753, P < 0.001). Post hoc analyses showed that there were significant differences between three groups at 3 d (sham: 38635.39 ± 2649.21 versus model: 17958.93 ± 1244.88 versus TMP: 19128.20 ± 1795.69; F = 205.913, P < 0.001), 7 d (sham: 38009.15 ± 2715.61 versus model: 22635.95 ± 2102.93 versus TMP: 25521.22 ± 1764.14; F = 80.61, P < 0.001), and 14 d (sham: 39059.86 ± 2831.29 versus model: 31203.85 ± 2478.53 versus TMP: 37147.30 ± 2168.38; F = 16.017, P < 0.001). Compared to sham group, rats in model group showed significantly lower expression of MAP-2 (3 d, 7 d, and 14 d all P < 0.001; decreased 53.52%, 40.45%, and 20.11%, resp.), although they exhibited an increasing trend from 3 d to 14 d after MCAO. TMP treatment resulted in upregulation in MAP-2 expression in peri-infarct area compared to model group at 14 d (P = 0.003; increased 19.05%) after MCAO.

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