ABSTRACT
ObjectiveTo investigate the effects of Anmeidan （AMD） on neuronal structure and neuronal marker protein expression in the hippocampal CA1 region of sleep-deprived （SD） rats. MethodRats were randomly divided into control group， model group， an AMD group （9.09 g·kg-1·d-1）， and melatonin group （0.27 g·kg-1·d-1）. Rats in the control group and the model group received equal volumes of physiologicol saline. The SD model was induced by the self-made sleep deprivation box for four weeks. Ethovision XT system detected and analyzed the spontaneous behaviors of rats. The histomorphology of neurons in the hippocampal CA1 region was observed by hematoxylin-eosin （HE） staining and Nissl staining， and the changes in Nissl bodies were observed by Nissl staining. The ultrastructure of hippocampal cells was observed by transmission electron microscopy （TEM）. Immunohistochemistry was used to detect the expression of glial fibrillary acidic protein （GFAP）， microtubule-associated protein 2 （MAP2）， nestin， and neuronal nuclei （NeuN） in the CA1 region. ResultCompared with the control group， the model group showed longer distance， increased average activity speed， cumulative duration， average body fill， and higher activity frequency （P<0.01）. Besides， the neurons in the CA1 region were reduced in number with disorganized arrangement， wrinkled nuclei， deeply stained cytoplasm， reduced Nissl bodies， swollen and deformed mitochondria， shortened cristae， and swollen Golgi vesicles. Furthermore， the mean integral absorbance （IA） value of GFAP increased and those of MAP2， nestin， and NeuN decreased （P<0.01）. Compared with the model group， the AMD group showed shortened distance traveled， lower average activity speed， shorter cumulative duration， decreased average body fill， and reduced activity frequency （P<0.05， P<0.01）. Moreover， the neurons in the CA1 region were relieved from damage with increased cell number， clear nuclei and cytoplasm， increased Nissl bodies， and relieved mitochondrial damage. The IA value of GFAP decreased and those of MAP2， nestin， and NeuN increased （P<0.05， P<0.01）. ConclusionAMD can improve structural damage of neurons in the hippocampal CA1 region of sleep-deprived rats， which may be achieved by decreasing GFAP expression and increasing MAP2， nestin， and NeuN expression.
ABSTRACT
Dexmedetomidine (Dex) has been demonstrated to provide neuroprotective effect against brain injury in the central nervous system. However, the underlying mechanism of this neuroprotection remains unclear. In this study, we explored whether Dex has the protective potential in rat models of traumatic brain injury(TBI). More importantly, our study further investigated the role of neuronic autophagy induced by PI3K/Akt/mTOR pathway in this neuroprotective action. Adult male Sprague-Dawley rats were subjected to a diffuse cortical impact injury caused by a modified weight-drop device and Dex (15ug/kg, i.v.) was administered immediately after TBI. Wet-dry weight method was used to evaluate brain edema. Motor function outcome was assessed by Neurologic Severity Score and the spatial learning ability was evaluated in a Morris water maze. The co-localization of microtubule-associated protein 1 light chain 3(LC3) and neuronal nuclei (NeuN), or LC3 and mammalian target of rapamycin (mTOR) were analyzed by immunofluorescence respectively. The expression of LC3, Phosphorylated protein kinase B (p-Akt) and p-mTOR were quantified using Western blot analysis. Our results showed treatment of rats exposed to TBI with Dex caused not only marked reduction in cerebral edema, motor and cognitive functions deficits, but also a decrease in LC3 levels and a increase in p-Akt and p-mTOR levels. Taken together, these findings indicated that treatment with Dex after TBI could inhibited neuronic autophagy in the hippocampus mediated by the activation of the PI3K/Akt/mTOR pathway, finally promoting neurological recovery.
ABSTRACT
Objective To study the effects of rehabilitation training on the regeneration of nerve cells in rats after intracerebral hemorrhage (ICH).Methods A total of 75 male SD rats were randomized into a training group,a control group and a sham operated group,25 rats/group.The ICH models were induced by stereotactical injection of collagenase type Ⅶ into the globus pallidus.The training group was trained with grasp,balancing and rotating exercise every day,the control group was restricted to their cages,and the sham operated group received normal saline injections.Each group was further subdivided into 1,4,7,14 and 28 day subgroups.Neurological function was measured in each group.Bromodeoxyuridine (BrdU) was used to label S phase cells,immunohistochemical single and double staining with antibodies against BrdU,microtubal-associated protein (MAP) and neuronal nuclei (NeuN) were used to determine neuronal proliferation,migration and differentiation in the subventricular zone ( SVZ ) and subgranular zone (SGZ) in the training and control groups.Results The motor function scores of the animals in the rehabilitation group were significantly lower than those of the control group.Proliferative BrdU + cells of the SVZ and SGZ in the control group rats were clearly less than those in the rehabilitation training rats at all time points.The results of the immunohistochemical double staining indicated that one week after ICH BrdU +/MAP + cells in the SVZ had increased significantly in the training group compared to the control group,and then decreased two weeks later.At the same time,BrdU +/MAP cells were found in the striatal boundary on the hemorrhage side,in numbers up to 8 times that in the control group.In the rehabilitation group striatal neuron differentiation on the hemorrhage side was 2 to 3 times that in the control group.Conclusion Rehabilitative training can enhance nerve cell proliferation,regeneration and neuron migration after ICH.