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1.
Chinese Journal of Pathophysiology ; (12): 1896-1900,1905, 2017.
Article in Chinese | WPRIM | ID: wpr-657750

ABSTRACT

AIM:To investigate the effect of ischemic postconditioning ( IPC) on autophagy induced by focal cerebral ischemia reperfusion ( I/R) in rats.METHODS:Healthy male SD rats were assigned randomly into sham-opera-tion (sham) group, I/R group and IPC group with 10 rats in each group.The rats in sham group were only exposed the right common , internal and external carotid artery surgically .The rats in I/R group were subjected to right middle cerebral artery occlusion (MCAO) by the modified Longa suture method for 2 h followed by 24 h of reperfusion.The rats in IPC group were subjected to MCAO for 2 h followed by reperfusion of the ipsilateral common carotid artery occlusion for 10 s for 5 episodes, and then reperfusion for 24 h.Autophagy was obeserved by transmission electron microscopy (TEM).The pro-tein levels of mammalian target of rapamycin (mTOR), p-mTOR and microtubule associated protein light chain 3 (LC3)-II in brain tissue of the rats were determined by Western blot .Pathological changes of brain tissue were observed by HE staining.RESULTS:The protein levels of mTOR and p-mTOR in IPC group were significantly higher than those in I/R group (P<0.05).The expression of LC3-II in IPC group was significantly lower than that in I/R group (P<0.01).The cerebral infarction area and brain water content in IPC group were significantly lower than those in I /R group (P<0.01). HE staining showed that neurons degeneration and necrosis in IPC group were significantly alleviated compared with I /R group.TEM observation showed that IPC revealed fewer autophagosomes , with much less severe cell damage than that in I/R group.CONCLUSION:IPC reduces brain ischemia reperfusion damage by decreasing autophagy of brain cells , which might be related to the activation of mTOR .

2.
Chinese Journal of Pathophysiology ; (12): 1896-1900,1905, 2017.
Article in Chinese | WPRIM | ID: wpr-660145

ABSTRACT

AIM:To investigate the effect of ischemic postconditioning ( IPC) on autophagy induced by focal cerebral ischemia reperfusion ( I/R) in rats.METHODS:Healthy male SD rats were assigned randomly into sham-opera-tion (sham) group, I/R group and IPC group with 10 rats in each group.The rats in sham group were only exposed the right common , internal and external carotid artery surgically .The rats in I/R group were subjected to right middle cerebral artery occlusion (MCAO) by the modified Longa suture method for 2 h followed by 24 h of reperfusion.The rats in IPC group were subjected to MCAO for 2 h followed by reperfusion of the ipsilateral common carotid artery occlusion for 10 s for 5 episodes, and then reperfusion for 24 h.Autophagy was obeserved by transmission electron microscopy (TEM).The pro-tein levels of mammalian target of rapamycin (mTOR), p-mTOR and microtubule associated protein light chain 3 (LC3)-II in brain tissue of the rats were determined by Western blot .Pathological changes of brain tissue were observed by HE staining.RESULTS:The protein levels of mTOR and p-mTOR in IPC group were significantly higher than those in I/R group (P<0.05).The expression of LC3-II in IPC group was significantly lower than that in I/R group (P<0.01).The cerebral infarction area and brain water content in IPC group were significantly lower than those in I /R group (P<0.01). HE staining showed that neurons degeneration and necrosis in IPC group were significantly alleviated compared with I /R group.TEM observation showed that IPC revealed fewer autophagosomes , with much less severe cell damage than that in I/R group.CONCLUSION:IPC reduces brain ischemia reperfusion damage by decreasing autophagy of brain cells , which might be related to the activation of mTOR .

3.
Chinese Journal of Zoonoses ; (12): 868-871, 2017.
Article in Chinese | WPRIM | ID: wpr-667740

ABSTRACT

To provide evidence for Campylobacter jejuni (C.jejuni) vaccine research,the B cell epitope of AhpC protein were predicted,and the antigenicity was analyzed.AhpC was found locating in outer membrane of C.jejuni without transmem brane structure and no signal peptide by bioinformatics software TMHMM Server V2.0,SignalP 4.1.There were seven B-cell linear epitopes in AhpC predicted by IEDB.Then,the AhpC protein and chemically synthesized antigenic epitopes of C.jejuni were used as antigens,and the AhpC antibody of C.jejuni was used as the primary antibody,the antigens of predominant linear B cell epitopes were detected by ELISA and dot blot.Results showed that one epitope of B cell epitopes (AhpC4-16) was able to recognize the antibodies of C.jejuni AhpC and had strong antigenicity,indicating that could be used in the follow-up vaccine research.

4.
Journal of Zhejiang University. Medical sciences ; (6): 272-277, 2010.
Article in Chinese | WPRIM | ID: wpr-259204

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effects of formaldehyde inhalation on the morphological damage, and Glu, GABA and NOS contents in olfactory bulb and hippocampus of rats.</p><p><b>METHODS</b>Twenty SD rats were equally divided into two groups: rats in the control group inhaled fresh air, while the animals in experimental group were exposed to the air containing formaldehyde (12.5 mg/m(3), 4 h/d) for 7 days. Then rats were sacrificed and frozen sections of olfactory bulb and hippocampus were prepared. The morphological changes were examined and the Glu, GABA and NOS contents were detected using Nissl-staining, immunohistochemistry and Western blot, respectively.</p><p><b>RESULT</b>Compared with the control group, there was a significant confusion and shrink of neuron morphology in experimental group, the number and staining intensity of Glu and NOS positive cells and protein contents were reduced. The protein expression of GABA was also decreased in the formaldehyde group.</p><p><b>CONCLUSION</b>Formaldehyde inhalation can cause a severe morphological damage of olfactory bulb and hippocampus in SD rats,which may further impair memory and learning ability through the reduction of Glu, GABA and NOS expression.</p>


Subject(s)
Animals , Rats , Formaldehyde , Toxicity , Glutamic Acid , Metabolism , Hippocampus , Metabolism , Pathology , Inhalation Exposure , Learning , Neurons , Metabolism , Pathology , Nitric Oxide Synthase , Metabolism , Olfactory Bulb , Metabolism , Pathology , Rats, Sprague-Dawley , gamma-Aminobutyric Acid , Metabolism
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