Figure 5.

Tuftsin fragment 1-3 decreased microglial activation and increased the survival rate of DA neurons. Tuftsin fragment 1-3 or artificial CSF was administrated into the contralateral lateral ventricle using mini-osmotic pump for 14 and 28 days. (A) Western blot assay of OX6 and ED1 in the ipsilateral SN at 14 dpl following unilateral MFB transection and administration of tuftsin fragment 1-3 or artificial CSF. (B) Quantification of results from western blot assay in (A). The density of each OX6 and ED1 band was normalized against that of beta-actin. Values were normalized to control and expressed as the mean ± S.E.M. (n = 3). *P < 0.05 compared with value from control and #P < 0.05 compared with value from sham control (ANOVA with post hoc Student’s t test). (C) OX6 and ED1 immunohistochemistry in the ipsilateral SN at 14 dpl following unilateral MFB transection. In vehicle treated animals (Sham), innumerable OX6-ir and ED1-ir microglia are crowed in the ipsilateral SN. However, in tuftsin fragment 1-3 treated animals (Tuft), the OX6 and ED1 immunoreactivities are deeply suppressed. Scale bar represents 250 μm. (D) Graph representing the relative percentage of the number of nigral TH-ir DA neurons. For quantitative analysis, every fourth section among 40 μm serial brain sections was immunohistochemically stained with antibodies against TH, and the number of TH-ir neurons were counted using a stereological technique in the whole SN. The percentage was analyzed by dividing the total number of TH-ir neurons in the ipsilateral SN by that of the contralateral SN. Values expressed as the mean ± S.E.M. (n = 7). *P < 0.05 compared with value from sham control (ANOVA with post hoc Student’s t test).

Song et al. BMC Neuroscience 2013 14:112   doi:10.1186/1471-2202-14-112
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