CREB phosphorylation in acupuncture combined with repetitive transcranial magnetic stimulation

Title: CREB phosphorylation in acupuncture combined with repetitive transcranial magnetic stimulation after cerebral ischemia endogenous activation of nerve regeneration and the mechanisms Author: Huang Fu Degree-granting units: Huazhong University of Science and Technology Key words: cerebral ischemia;; EA;; repetitive transcranial magnetic stimulation;; protein kinase A-cAMP response element binding protein;; electric platform; Neodymium Magnets cerebral ischemia;; power
Needle;; repetitive transcranial magnetic stimulation;; more sialic acid neural cell adhesion molecule;; neurons;; calcium-binding protein Abstract:

 The first part, PKA-CREB signaling pathway in the electro-acupuncture combined with repetitive transcranial magnetic stimulation after cerebral ischemia endogenous activation of nerve regeneration
The role and mechanism

 Objective:

 Of PKA-CREB signaling pathway in the EA (electro-acupuncture, EA) results
Combined repetitive transcranial magnetic stimulation (repetitive Transcranial Magnetic Stimulation, rTMS) after cerebral ischemia endogenous activation
Nerve regeneration and its mechanism.

 Methods:

 150 Wistar rats were obtained using rat intraluminal
Middle cerebral artery occlusion model [Liaowei Jing, Liu Shuhong, Fan, et al. Suture blocking the middle cerebral artery produced ischemic brain injury model
Type of improvement. Journal of Physical Medicine and Rehabilitation, 2002,24 (6) :345-349. ], Randomly divided into normal group, model group, EA
Group, rTMS group and EA + rTMS group, by immunohistochemistry and Western blot detection of brain ischemia after 7d, 14d and 28d is not the same three
Phase in rat ischemic hippocampus PKA, pCREB expression changes, and observing the neurological score and learning and memory.

 Research results
Fruit:

 (1) EA group, rTMS group and EA + rTMS group at each time neurological score and power down test score improvement compared with model group (p <
0.01, p <0.05), especially EA + rTMS group is obvious;

 (2) after ischemia at different time and ipsilateral hippocampal PKA
The positive expression of pCREB and the gray value in model group than in the normal group at 7d, 28d, when less than the normal group, the differences were statistically significant
Yi (p <0.05), 14d when http://www.everbeenmagnet.com/en/products/110-sintered-neodymium-magnets compared with the normal group the difference was not statistically significant (p> 0.05); EA group, rTMS group and EA + rTMS group of three
Phase were higher than the model group, 7d, 14d is higher than the normal group, the difference was statistically significant (p <0.05), 28d worse when compared with the normal group
No statistically significant differences (p> 0.05); EA + rTMS group 7d, 14d is higher than the EA group and the rTMS group, the difference was statistically significant (p <0.
05), EA group and the rTMS group at each time the difference was not statistically significant (p> 0.05);

 (3) pCREB expression and proliferation of NSCs into the amount of
Positive correlation.

 Findings:

 EA combination of rTMS on ischemic recovery of neurological function after stroke has a significant promotion of
Role in ischemic hippocampal PKA-CREB expression of signaling molecules may be the treatment of one of the mechanisms of ischemic stroke.

 
The second part, electro-acupuncture combined with repetitive transcranial magnetic stimulation on focal cerebral ischemia endogenous neural stem cell migration and differentiation

 
Objective:

 Of EA (electro-acupuncture, EA) with repetitive transcranial magnetic stimulation (repetitive
TranscranialMagnetic Stimulation, rTMS) on focal cerebral ischemia endogenous neural stem cell migration, differentiation
And its treatment of ischemic brain injury mechanisms.

 Methods:

 Take 120 Wistar rats, using the suture method
Middle cerebral artery occlusion rat model [Liaowei Jing, Liu Shuhong, Fan, et al. Suture blocking the middle cerebral artery produced ischemic
Brain injury model improvements. Journal of Physical Medicine and Rehabilitation, 2002,24 (6) :345-349. ], Randomly divided into normal group, model
Type group, EA group, rTMS group and EA + rTMS group, the use of dynamic testing by immunohistochemistry after cerebral ischemia 7d, 14d and 28d
Three different time, different brain regions and more sialic acid neural cell adhesion molecule (polysiolylated neural cell adhesion
molecule, PSA-NCAM) and PSA-NCAM/5- olfactory deoxyuridine (5-bromodeoxyuridine, BrdU), nucleus antigen
(Neuronalnuclear antigen, NeuN) and NeuN / BrdU, calcium-binding protein (Calbindin) and other markers of immune-positive form
Up.

 The results:

 (1) PSA-NCAM in the normal group only a few sparse expression, staining pale; 7d after ischemia, the positive fine
Cells was significantly increased (P <0.05), cluster-like distribution, processes short, 14d expression reached a peak, larger cell body, neurite longer, 28d
Expression began to decline; PSA-NCAM/BrdU a small amount of labeled cells in the normal expression, 7d after ischemia increased expression (P <0.05), 14d
Expression reached a peak, 28d expression decreased, still higher than the normal group (P <0.05). EA group, rTMS group, EA + rTMS group and model group at 7d
, 14d when the differences were statistically significant (P <0.05), EA + rTMS group and the EA group, rTMS group at 7d, 14d when the difference is also statistically
Significance (P <0.05), EA group, rTMS group, EA + rTMS group and model group at 28d and PSA-NCAM/BrdU compared to PSA-NCAM-positive fine
The number of cells was no significant difference between (P> 0.05);

 (2) NeuN sparse in the normal group only a small amount of expression, ischemia
7d after positive cells was significantly increased (P <0.05), 14d expression reached a peak, 28d expression began to decline; NeuN / BrdU labeled
Recorded cells in the normal group is almost no expression, 7d after ischemia increased expression (P <0.05), 14d expression reached a peak, 28d expression decreased,
Still higher than the normal group (P <0.05). The most significant increase for the EA + rTMS group, EA group and the rTMS group also had significantly increased in model group increased
At least; from between the two groups to see, EA group, rTMS group, EA + rTMS group and model group at 7d, 14d when the differences were statistically significant (P <0
. 05), EA + rTMS group at 7d, 14d, and when the rTMS group were higher than the EA group (P <0.05), EA group, rTMS group, EA + rTMS group and model
In the 28d group compared to NeuN and NeuN / BrdU positive cells was no significant difference between (P> 0.05);

 (3) is
Rat brain tissue normally seen Calbindin-D28k-positive neurons expressed a clear, neat layer of neurons and dense, form is
Often, more than neuronal expression, stained dark. Model group biopsy shows Calbindin-D28k-positive neurons shrink, disordered arrangement of neurons
Chaos and loose, stained lighter, less expression. EA + rTMS group sections Calbindin-D28k-positive neurons have more expression, form the base
The normal cells stained darker. EA group, rTMS group sections showed that Calbindin-D28k-positive neurons express unclear, cell morphology
Irregular, showing ischemic necrosis, fewer positive cells, stained lighter. EA group, rTMS group at each time and EA + rTMS Group 7d
, 14d when the Calbindin-D28k expression are less than the normal group (P <0.05), EA + rTMS group section 28d and the normal group showed no statistical
Significance (P> 0.05), EA group, rTMS group, EA + rTMS group at each time Calbindin-D28k expression was higher than the model group (P <0
. 05), EA + rTMS group at each time Calbindin-D28k expression was higher than the EA group, rTMS group (P <0.05), EA group and the rTMS group
Between each phase was no significant difference (P> 0.05). Each group SVZ, SGZ all time Calbindin-D28k expression was higher than
Around the cortical infarct.

 Findings:

 EA combination of rTMS for the different brain regions of ischemic neural stem cells derived
Proliferation, migration and differentiation and integration, and promote nerve regeneration and functional recovery after nerve injury may be the treatment of ischemic stroke
Important role in one of the mechanisms. Degree Year: 2009