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1.
Chinese Journal of Applied Physiology ; (6): 27-30, 2009.
Article in Chinese | WPRIM | ID: wpr-252717

ABSTRACT

<p><b>AIM</b>To study the expression and effect of TLR4 and NFkappaB protein in hippocampus neuron in rats exposed to chronic hypoxic hypercapnia.</p><p><b>METHODS</b>The disorder of learning-memory in pulmonary hypertension rat model was reproduced by chronic hypoxic hypercapnia. Thirty rats were randomly divided into three groups: normal control group, hypoxic hypercapnia 2-week and 4-week group. The number of apoptosis neurons in hippocampus CA1/3 was counted by TUNEL method. Activity of TLR4 and NFkappaB in hippocampus CA1/3 was detected by using SP immunocytochemical technique.</p><p><b>RESULTS</b>The expression of TLR4 protein in hippocampus CA1/3 in group 2HH( CA1: 0.1275 +/- 0.0242, CA3: 0.1156 +/- 0.0376) and 4HH (CA1: 0.1522 +/- 0.0187, CA3: 0.1427 +/- 0.0453) were significantly higher than those in the NC group (P < 0.05, P < 0.01). The positive expression of NFkappaB were showed in cell nucleus in group 2HH (CA1: 0.1326 +/- 0.0324, CA3: 0.1301 +/- 0.0112) and group 4HH (CA1: 0.1612 +/- 0.0428, CA3: 0.1578 +/- 0.0365), and significantly higher than those in the NC group (P < 0.05, P < 0.01). The apoptosis of neural cells in hippocampus CA1/3 gradually increased with the time of exposure, and reached peak at 4 weeks (P < 0.01 vs NC group).</p><p><b>CONCLUSION</b>The activation of TLR4 and NFkappaB may play an important role in the apoptosis of hippocampus neural cells in rat exposed to chronic hypoxic hypercapnia.</p>


Subject(s)
Animals , Male , Rats , Apoptosis , Hippocampus , Metabolism , Pathology , Hypercapnia , Metabolism , Hypertension, Pulmonary , Metabolism , Hypoxia , Metabolism , NF-kappa B , Metabolism , Neurons , Metabolism , Physiology , Random Allocation , Rats, Sprague-Dawley , Toll-Like Receptor 4 , Metabolism
2.
Chinese Journal of Applied Physiology ; (6): 434-437, 2007.
Article in Chinese | WPRIM | ID: wpr-253383

ABSTRACT

<p><b>AIM</b>To explore the effect of chronic hypoxic hypercapnia on learning-memory and the possible mechanisms involved.</p><p><b>METHODS</b>Fifty-eight male SD rats were randomly divided into three groups: Normal control group (NC, n=18), 2-week (2HH, n=18), and 4-week hypoxic hypercapnia (4HH, n=20) group. The rats, spatial learning-memory tasks were assessed by the Morris water maze. The expression of NMDAR1mRNA was determined by hybridization in situ.</p><p><b>RESULTS</b>Compared with NC group, rats exposed to chronic hypoxic hypercapnia displayed significant impairment in their performance assessed by two measures: mean escape latencies (2HH: 38.59 +/- 8.35 s, 4HH: 60.59 +/- 17.28 s) and swim path distances(2HH: 9893.45 +/- 1958.16 mm, 4HH: 18077.57 +/- 6878.85 mm). The expression level of NMDAR1mRNA in the hippocampus and cortex were lower than those in the NC group, especially, the NMDAR1mRNA expression of hippocampus CA1 in 4HH decreased by 21.4% (P < 0.01).</p><p><b>CONCLUSION</b>Chronic hypoxic hypercapnia could impair the rat spatial learning-memory and the decrease in expression of NMDAR1mRNA might be involved in.</p>


Subject(s)
Animals , Male , Rats , Hypercapnia , Metabolism , Hypoxia , Metabolism , Maze Learning , Memory , Rats, Sprague-Dawley , Receptors, N-Methyl-D-Aspartate , Metabolism
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