Role of Bcl-2 adenovirus/E1B 19kD interacting protein 3 in oligodendrocyte apoptosis after diffuse axonal injury / 解剖学报

Objective To investigate the role of Bcl-2 adenovirus/E1B 19kD interacting protein 3 (BNIP3) in oligodendrocyte apoptosis after diffuse axonal injury (DAI) in rats. Methods Seventy-seven male adult Sprague-Dawley rats were randomly divided into sham group (n = 11), DAI group (n = 33), and intervention group (n = 33). DAI model was made referring to modified Marmarou method and the rats in intervention group received intracerebroventricular injection of BNIP3 inhibitor, necrostatin-1 (Nec-1, 30 g/L, 2 μl) immediately after injury. Tested the BNIP3 protein expression, oligodendrocyte apoptosis and myelin histopathology before and after the intervention of Nec-1. Results Compared with the sham group, DAI rats upregulated BNIP3 levels and had positive correlation with cell apoptosis in brainstem. Nec-1 significantly inhibited BNIP3 expression, then decreased the number of apoptotic oligodendrocytes, increased the average absorbance of luxol fast blue (LFB) staining and myelin basic protein (M BP) levels, and alleviated the myelin ultrastructure of DAI rats. Conclusion BNIP3 participate in the DAI-induced apoptosis of oligodendrocytes, and inhibition of BNIP3 can protect oligodendrocytes and myelin sheath from DAI injury.

Glial response following diffuse axonal injury / 解剖学报

Objective To explore the glial response and the relationship with secondary axonal degeneration in rats after diffuse axonal injury (DAI). Methods Adult male Sprague-Dawley rats were randomly assigned to control or DAI groups sacrificed at 1, 2, 3, 5 and 7 days with 10 rats in each group. DAI model was made referring to modified Marmarou method and glial fibrillary acidic protein (G F A P), ionized calcium binding adaptor molecule-1 (Ibal), recombinant oligodendrocyte lineage transcription factor 2 (Olig2), CC-1, NG2 immunohistochemistry, TUNEL staining and transmission electron microscopy were performed in brain stem. Results The number of Ibal labeled positive cells was significantly increased at day 3 and day 7 after injury. Moreover, different hypertrophic morphology was identified after injury. There was no effect of DAI on GFAP expression in brain stem. Numbers of mature oligodendrocyte marker CC-1 immunoreactivity cells within brain stem were significantly decreased at each of the time points after injury. The number of TUNEL positive cells in brain stem was significantly increased with injured time. Olig2 expression was significantly increased throughout the first week and reached peak at day 3 after injury in brain stem. The number of NG2 labeled positive cells was significantly increased at day 3 and day 7 after DAI. Ultrastructural evidence showed myelin release then further developed as widespread delamination and collapse, and leading to degeneration of axonal partner. Conclusion Mature oligodendrocytes are vulnerable in DAI and myelin loss may contribute to axonal degeneration. OPCs proliferate with activation of microglia. This insight of glial response will further explain the pathophysiological mechanism of secondary axonal damage in DAI.

Effects of high and low shear stress on vascular remodeling and endothelial vascular cell adhesion molecular-1 expression in mouse abdominal aorta / 南方医科大学学报

<p><b>OBJECTIVE</b>To establish a mouse model of abdominal aorta stenosis and analyze the alterations in the arterial wall response to high and low shear stress.</p><p><b>METHODS</b>Twenty mouse were randomized equally into 4 groups, including 3 test groups (1, 7 and 14 day groups) with surgically induced stenosis of the abdominal aorta, and a sham-operated group without stenosis. The hemodynamics and the internal diameter of the blood vessel were measured by color Doppler flow imaging. The wall shear stress was calculated by Poiseiulle hydrodynamics formula (τ(m)=η×4×V(m)/D). Pathological examination and immunohistochemistry were performed to observe the arterial morphological changes and the endothelial vascular cell adhesion molecule-1 (VCAM-1) expression. The intimal-media thickness of the aorta was measured and endothelial VCAM-1 expression analyzed quantitatively.</p><p><b>RESULTS</b>Regions of low and high flow shear stress were created upstream from the stenosis and within the stenosis, respectively. Compared with the sham-operated group, the mice with aorta stenosis showed gradually increased vascular intimal-media thickness and VCAM-1 expression intensity in the upstream aorta, but not within the regions of the stenosis.</p><p><b>CONCLUSION</b>Vascular remodeling may occur shortly after exposure to low shear stress, which plays a significant role in initiation and progression of the pathological process of atherosclerosis mediated by VCAM-1, whereas high shear stress may exert an anti-atherosclerotic effect.</p>

Relationship between myocardial systolic, diastolic functions and perfusion in coronary artery stenosis / 南方医科大学学报

<p><b>OBJECTIVE</b>To evaluate the relationship between myocardial systolic, diastolic functions and perfusion in coronary artery stenosis using velocity vector imaging (VVI) and myocardial contrast echocardiography (MCE).</p><p><b>METHODS</b>Stenoses in the anterior descending branch of the coronary artery were induced in 8 dogs. Before and after coronary artery stenosis, two-dimensional images of the left ventricular mastoid muscle section on the short axis at rest and in the peak dose of dobutamine were obtained for evaluation of VVI and MCE. The myocardial blood flow A.beta values, peak systolic strain rate (SRsys) and peak diastolic strain rate (SRdia) in the direction of the circumference of the short axis were measured.</p><p><b>RESULTS</b>At rest, only severe coronary stenosis resulted in significantly lowered SRsys, SRdia and A.beta value of the stenotic bed compared to the values before the stenosis (-1.1-/+0.50 vs -1.62-/+0.50, 1.19-/+0.48 vs 1.75-/+0.51, 0.4-/+0.21 vs 0.80-/+0.47, P<0.05). In stress, SRsys, SRdia and A.beta value of the stenotic bed gradually decreased as coronary stenosis worsened (-4.31-/+1.14 vs -3.20-/+0.98 vs -1.18-/+0.64, 4.51-/+1.13 vs 3.39-/+0.98 vs 1.37-/+0.64. 3.54-/+1.95 vs 1.81-/+0.89 vs 0.82-/+0.42, P<0.05). Both at rest and in stress, good correlations were noted between SRsys and SRdia (r(rest)=0.88, r(stress)=0.96, P<0.01), between SRsys and the standard A.beta values (r(rest)0.56, r(stress)=0.71, P<0.01), and between SRdia and A.beta (r(rest)=0.57, r(stress)=0.72, P<0.01) in the direction of the circumference of the short axis.</p><p><b>CONCLUSIONS</b>Using VVI and MCE, the changes in myocardial perfusion and the systolic and diastolic functions in the direction of the circumference can be observed dynamically. VVI may help assess the condition of myocardial perfusion by evaluating the systolic and diastolic function.</p>