ABSTRACT
<p><b>OBJECTIVE</b>To examine whether ischemic preconditioning (IPC) can protect neuron against delayed death in CA1 subfield of hippocampus following reperfusion of a lethal ischemia in rats, and explore the role of p53 and bax in this process.</p><p><b>METHODS</b>We examined the effect of IPC on delayed neuron death, neuron apoptosis, expressions of p53 and bax gene in the CA1 area of hippocampus in the rats using HE staining, flow cytometry, RT-PCR, and immunohistochemistry technique.</p><p><b>RESULTS</b>IPC enhanced the quantity of survival cells in the CA1 region of hippocampus (216 +/- 9 cells/0.72 mm2 vs. 30 +/- 5 cells/0.72 mm2, P < 0.01) , decreased the percentages of apoptotic neurons of hippocampus caused by ischemia/reperfusion (2.06% +/- 0.21% vs. 4.27% +/- 0.08%, P < 0.01 ), and weakened the expressions of p53 and bax gene of hippocampus compared with ischemia/reperfusion without IPC.</p><p><b>CONCLUSION</b>IPC can protect the neurons in the CA1 region of hippocampus against apoptosis caused by ischemia/reperfusion, and this process may be related to the reduced expressions of p53 and bax.</p>
Subject(s)
Animals , Rats , Gene Expression Regulation , Genes, p53 , Hippocampus , Wounds and Injuries , Ischemic Preconditioning , Methods , Neurons , Physiology , Reperfusion Injury , Tumor Suppressor Protein p53 , Genetics , bcl-2-Associated X Protein , GeneticsABSTRACT
To investigate the changes in bcl-2, bax expression and neuron apoptosis in the hippocampus after the blockade of cervical lymphatics, the model of lymphostatic encephalopathy was established by occluding and removing both the superficial and deep cervical lymph nodes in rats. The animals were sacrificed at 1, 2, 3, 5, 7 and 14 d after operation. H and E staining was used to observe the structure of brain tissues and TUNEL staining was used to detect in situ cell apoptosis in the hippocampus. The expression of bcl-2 and bax in the hippocampus were examined by RT-PCR. The results showed that cerebroedema appeared at day 2 and was most serious at day 5 after the blockade of cervical lymphatics. The number of TUNEL positive cells began to increase at day 2 and reached the maximum at day 5. The expression of bax began to increase at day 1 and reached the maximum at day 2. The expression of bcl-2 began to decrease at day 1 and dropped to the minimum at day 5. The items mentioned above recovered to control level at day 14. These results suggest that lymphostatic encephalopathy following the blockade of cervical lymphatics result in changes in bcl-2 and bax expression in the hippocampus and that apoptosis is the main form of neuron death.
Subject(s)
Animals , Female , Male , Rats , Apoptosis , Physiology , Hippocampus , Metabolism , Pathology , Lymph Node Excision , Lymphatic System , Physiology , Neck , Neurons , Cell Biology , Proto-Oncogene Proteins c-bcl-2 , Genetics , Metabolism , Random Allocation , Rats, Wistar , bcl-2-Associated X Protein , Genetics , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate effects of total flavonoid fraction of Asttragalus complanatus on blood pressure in conscious spontaneously hypertensive rats(SHR) and hemodynamics in anesthetized SHR.</p><p><b>METHOD</b>Blood pressure was recorded with tail-culf method and hemodynamics was recorded with polygraph after administration of total flavonoid fraction of Asttragalus complanatus.</p><p><b>RESULT</b>Total flavonoid fraction of Asttragalus complanatus (100, 200 mg.kg-1) could decrease blood pressure of conscious SHR(decreasing 7.1%, P < 0.05 and 9.3%, P < 0.01 respectively). Meanwhile, there was no significant change in heart rate(HR). R Br (200 mg.kg-1) could decrease total peripheral resistance (TPR) (decreasing 20%, P < 0.05) but did not influence the cardiac output(CO) and heart rate in anesthetized SHR.</p><p><b>CONCLUSION</b>Total flavonoid fraction of Asttragalus complanatus possesses obvious hypotensive effect, mainly by means of decreasing the TPR.</p>