兰州大学机构库 >学院待认领
大鼠颅脑损伤并发急性胃粘膜病变时PAF与ET-1作用机制的实验研究
Alternative TitleExperimental study on roles of PAF and ET-1 in acute gastric mucosa lesion following traumatic brain injury in rats
刘国胜
Subtype硕士
Thesis Advisor任海军
2007-03-21
Degree Grantor兰州大学
Place of Conferral兰州
Degree Name硕士
Degree Discipline神经病学
Keyword颅脑损伤 急性胃粘膜病变 溃疡指数 内皮素1 放射免疫 免疫组化 血小板活化因子
Abstract目的 通过动物实验检测血中PAF与ET-1的浓度变化及胃粘膜ET-1的表达,探讨PAF与ET-1在大鼠颅脑损伤并发急性胃粘膜病变时的意义及作用机制。材料和方法Wistar雄性健康大鼠70只,随机分为正常对照组(10只),假损伤组(10只)和损伤组(50只),损伤组又分为4、12、24、72小时﹑5天等5个时相点(每个时相点10只),制造大鼠颅脑损伤模型,应用放免、免疫组化、酶免疫及病理切片技术,动态检测各组血中PAF和ET-1浓度、溃疡指数(UI)、胃粘膜细胞镜下形态学变化及ET-1在大鼠胃粘膜组织中的分布与表达。结果①血液中PAF水平颅脑损伤后4小时开始升高(P<0.01),24小时达到高峰,与正常组比较P<0.01。随后开始下降,5天后恢复正常。②损伤组大鼠血浆ET-1浓度与正常对照组和假损伤组相比明显升高。于12小时达到高峰(P<0.01),且随着血浆ET-1水平的不断升高,伴有UI明显增加;ET-1水平于伤后12小时开始下降,但仍高于正常对照组,5天后达到正常水平。③胃粘膜溃疡指数(UI)在颅脑损伤后明显增加(P<0.01),24小时增加最为明显,5天后下降至正常水平。④免疫组化研究显示:损伤后ET-1阳性细胞表达数量与强度明显增加,主要分布在胃粘膜上皮细胞、胃粘膜肌层血管内皮细胞及血管与胃壁的平滑肌细胞等组织细胞的胞浆中。假损伤组表达无明显变化。结论本研究得出如下结论:①在大鼠颅脑损伤并发急性胃粘膜病变过程中,血中PAF、ET-1含量明显升高,胃粘膜组织中ET-1表达增强,且血浆ET-1含量与胃粘膜溃疡指数(UI)呈正相关(P<0.01)。提示PAF和ET-1可能参与颅脑损伤并发急性胃粘膜病变的形成。②PAF的可能作用机制主要是引起胃粘膜血管通透性增加、胃粘膜屏障破坏。③ET-1的可能作用机制主要是造成胃粘膜血流量下降,导致胃粘膜微循环障碍。④早期补充外源性PAF与ET-1拮抗剂,可能减轻急性胃黏膜病变的程度及发生率。
Other AbstractObjectives To explore the significance and mechanism of PAF and ET-1 during acute gastric mocusa following traumatic brain injury(TBI) by observing the changes of serum platelet-activating factor (PAF),plasma endothelin(ET)-1 level and the expression of ET-1 in gastric mucosa at different time phases after TBI in rat models. Methods 70 healthy adult Wistar rats were randomly divided into normal control group, sham-injuried group, and traumatic brain injury groups at hour 4,12,24,72 and at day 5 post-trauma(each group 10 rats), then made the models of traumatic brain injury. The serum level of PAF in each group were examined by ELISA methods and the level of ET-1 in plasma was examined by radioimmunoactive(RIA). The stomach of the rats were removed for observing condition of gastric mucosa and the expression of ET-1 on gastric mucosa in each group by immunohistochemistry(IHC). Results The serum level of PAF and ET-1 in normal control group and sham-injuried group was no significant on statistics difference; The level of PAF in serum increased from hour 4 post-trauma and reached a peak at hour 24, then drop to the normal level at day 5 after brain injury. The level of ET-1 in plasma significantly increased in injury groups compared with the normal control group and sham-injury group and showed a peak at the 12th hour postinjury (P<0.01), then begins to decrease thereafter the 12th hour, but remains a higher level than normal control group, which reaches normal level at day 5. In addition, UI increased dramatically at the 4th hour (P<0.01) and reach a maximum value at the 24th hour then reached normal level at the 5th day after brain injury. The expression of ET-1 was stained as brownish grains and localized in the cytoplasma of gastric epithelial cells, vascular endothelium cells, vascular smooth muscule cells and stomach smooth muscle cells, both the proportion and cellular intensity of ET-1 positive cells were significantly higher in traumatic brain injury group than in normal control group. The expression of ET-1 in sham-injuried group is the same with normal control group.Conclusion The results indicate that: The level of ET-1 in plasma and PAF in serum increased after traumatic brain injury, at the same time the expression of ET-1 on gastric mucosa were also enhanced. Furthmore the level of ET-1 in plasma related to with UI. Both ET-1 and PAF aggravated acute gastric mucosa lesion by decreasing blood flow, affecting microcirculation of gastric mucosa and increasing the vasopermeability, deteriorating the barrier of gastric mucosa respectively. Replenishment of ET-1 and PAF antagonist may relieve extent and incidence rate of AGML in early phase after brain injury.
Pages46
URL查看原文
Language中文
Document Type学位论文
Identifierhttps://ir.lzu.edu.cn/handle/262010/341619
Collection学院待认领
Affiliation临床医学院
Recommended Citation
GB/T 7714
刘国胜. 大鼠颅脑损伤并发急性胃粘膜病变时PAF与ET-1作用机制的实验研究[D]. 兰州. 兰州大学,2007.
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