| Wistar rats of 7-oId were random1y divided into three groups: hypoxic-ischemic(Hl)group, HI-cerebrolysin-treated group and control group. The rats of HI group and Hl-cerebrolysin-treated group underwent uniIateral common carotid artery Iigation and exposedto hypoxic state (8% oxygen +92% nitrogen ) in order to set newborn rat hypoxic-ischemicencephalopathy (HlE) model. The rats of HI-cerebrolysin-treated group were immediateIyinjected with cerebrolysin to therapy once everyday for four days after hypoxia-ischemia.The three groups rats were made dead at 6, 24, 72 and 96 hour after hypoxia-ischernia bycutting head and the brain tissues were separately taken. Radioimmunoassay, biochemicaltechnique, transmission electron microscope technique, pyronin and methyl green (PMG)staining and hematoxylin and eosin (H.E) staining were used to meature dynamic changes ofthe content of tumor necrosis factor- Q (TNF- Q ), interleukin-l D (lL-l 6 ), thromboxaneBz(TXBz), 6-keto-prostaglandin Fl o (6-keto-PGFl o ) and malondialdehyde (MDA), theactivity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and thenumber of apoptosis cell and to eva1uated the changes of histopathological morphology ofleft brain tissue. The content of water was meatured in right brain tissue. The purpose is toreveaI the pathogenesis of hypoxic-ischemic encephalopathy in newborn rat and the effectsand mechanism of treatment with cerebroIysin on hypoxic-ischemic encephalopathy innewborn rat and to search a economic and effective pathway of therapying hypoxic-ischemicencepha1opathy in neonataI cIinic.The results were as fo1lows:l The content of TNF- Q and IL-l 6 increased significantly in brain tissue of hypoxic-ischemic newborn rats as compared with those of control groups. The result showed thatcytokine participated brain damages of hypoxic-ischemic encephalopathy in newborn rat.2 The content of TXB2 and 6-keto-PGF1. and the ratios of T/P increased markedly inbrain tissue of hypoxic-ischemic newborn rats as compared with those of control groups.The result showed that the changing of cerebral blood was one of the main reasons whichinduced brain damages by making unbalance of TXA2-PGI2 system after hypoxia-schemia in newborn rat.3 The content of MDA increased significantly and the activity of SOD and GSH-Pxdecreased markedly in brain tissue of hypoxic-ischemic newborn rats as compared withthose of control groups. The result showed that hypoxia-ischemia made the oxidationIland oxidation prevention system losing baIance so that oxygen free radicaIs generatedexcessively and brain damages happened.4 The number of apoptosis celIs were significantly higher than those of control group inbrain tissue of hypoxic-ischemic newborn rats. The result certified that the braindamages of hypoxic-ischemic encephalopathy had close relationship with cell apoptosisin newborn rat.5 The content of water were higher than those of control group in right brain tissue ofhypoxic-ischemic newborn rats. The result showed that local cerebral hypoxia andischemia caused brain damages not only in local cerebra but also in who1e cerebra.6 After the treatment with cerebrolysin, the content of TNF- Q, lL-l P, TXB2, 6-keto-PGFl., MDA, the number of apoptosis ce1l and water decreased and the activity ofSOD and GSH-Px enhanced significantly in brain tissue of HI-cerebrolysin-treated groupas compared with those of HI group. The results indicated that cerebroIysin hadtreatment effects on hypoxic-ischemic encephalopathy in newborn rat by suppressingexcessive expression of cytokine, improving brain blood, repressing production ofoxygen free radicaIs, enhancing activity of antioxidant enzyme and reducing number ofapoptosis cell and brain edema of hypoxic-ischemic encephaIopathy in newborn rat.Postgraduate: Zhang Rui LiSupervisor: Professor Zhcng Shi MinSpeciality: Basic Vcterinary... |
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