Study On The Level Of NO,TNF-α,MDA,SOD In Cerebrospinal Fluid From Patients With Cysticercosis | | Posted on:2003-10-25 | Degree:Master | Type:Thesis | | Country:China | Candidate:L K Wu | Full Text:PDF | | GTID:2144360065950195 | Subject:Pathogen Biology | | Abstract/Summary: | PDF Full Text Request | | Purpose : Cerebral cysticercosis is a common but severe disease caused by encystment of the larvae of Taenia soliun in central nervous system.The main mechanism that lead to neuron injury is the immune-inflammatory reaction which causes metabolic acidosis,intracellular calcium ion (Ca2+) overload,excitating amino acid (EAA) toxity,lipoid metabolic disorder and oxygen radical mediating cell death,etc.While Ca2+ influx increase is not only the result of acidosis and radical attack but the start-up factor of radicals producing and many enzymes overactivity(for example TXA2).An excessive accumulation of nitric oxide (NO) mediates EAA release cascade that results in intracellular Ca2+ persistent increase.These reactions aggravate neuron injury and give rise to the host's killing cysticercus.Super oxide dismutase (SOD) is a major defense mechanism against radicals and it's activity was reported to decrease in patient with cerebral cysticercosis.When SOD is suppl dlfhis ability to clean radicals is improved, and the injury of microcirculation vascular endotheliocyte and neuron are attenuated.At the same time SOD has an inhibitory effect ondisinsection in vivo.Based on taenia living stage the cerebral pathological changes are devided into four stages.lt is important to analyze the biochemical changes and their relations with immuno agents in different pathological stage.lt has been demonstrated that NO play an important role as an effector molecule in the control of the cerebral cysticercosis. However,the precise mechanisms by which it mediates an effect in vivo is not known and the importance of this molecule for the development of cerebral cysticercosis is debated.Tumor necrosis factor alpha (TNF- a ) malondialdehyde (MDA) and SOD are related to the level of NO. To assess whether cerebral cysticercosis is NO dependent, we measured the level of NO TNF- a MDASOD in patients cerebrospinal fluid(CSF), sought to provide additional insights in the role of NO, cytokine and free radicals in parasite infection.Methods: Forty-nine patients with cerebral cysticercosis and twenty normal controls paticipated in the study. Based on clinical symptoms immunological and magnetic resonance imaging(MRI) results, patients were divided into four stages, including the alive cysticercus stage(11 cases), the early degeno-death stage(14 cases), the late degeno-death stage(10 cases) and the calcification (static) stage(14 cases). After regular exemination,the CSF samples were stored under -20 癈 . Cysticercus counter immuno-electrophoresis tests were examined before stage-dividing.The level of NO TNF- a, MDA and SOD in CSF were detacted. The data were analyzed with the software of SPSS in personal computer.Results: (1) There was no positive result of cysticercus counter immunoelectrophoresis in the controls while in the patient groups the positive rate in four stages were respectively 27% 85.7%. 80%, 76.3%, in which the 2-4 stages had significantly higher levels. (2) The level of TNF-a rised earlier than NO.The amout of NO was decreased in the first stage and greatly increased in the second and third stages,went back to the normal level in the last stage. (3) The level of TNF- a and MDA were both increased in the four stages of the patients,and reached the peaks in the second stage. (4) Compared with control group,the activity of SOD in patient groups were reduced, and the difference was statistically significant. (5) SOD had a negtive correlation with NO, TNF- a and MDA.There were positive correlations among NO, TNF-a and MDA.Conclusions: The data suggest that NO may be parasiticidal in the development of cerebral cysticercosis in vivo, there is a dynamic banlance between the immuno regulation and anti- cysticercus roles of NO. TNF- a may participate in the control of infection depending on the cysticercus antigen. Oxygen free radicals genesis, as post-receptor reaction of TNF- a , is suggested to be one of the main mechanisms of parasite killing. MDA has a negativecorrelation with SOD.SOD is a major free radical... | | Keywords/Search Tags: | cerebral cysticercosis nitric oxide(NO), tumor necrosis factor alpha (TNF-α), malondialdehyde (MDA), superoxide dismutase (SOD) | PDF Full Text Request | Related items |
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