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目的:以内毒素休克脑损伤的研究为切入点,对内毒素休克大鼠脑组织肿瘤坏死因子-α(TNF-α)及超氧化物歧化酶(SOD)含量的规律性变化进行分析,探求不可逆休克时微循环障碍的中枢变化过程,为急症救治技术提供新的途径。方法:选用体质量180-200g的6-8周龄SD大鼠72只,随机分为假手术组、模型组与四逆汤组,每组24只。建立内毒素休克大鼠模型,采用ELISA法测定脑组织TNF-α含量,分光光度法进行SOD定量测定,检测并分析各组大鼠脑组织1、2、3、6h不同时间段的TNF-α及SOD含量。结果:①内毒素休克后模型组大鼠脑组织中TNF-α含量于6h达峰值,模型组与假手术组比较各时间段均明显升高(P<0.01),四逆汤组与模型组3、6h时间段比较明显下降(P<0.05或P<0.01)。②内毒素休克后模型组大鼠脑组织中SOD含量于6h达峰值,模型组与假手术组比较各时间段均明显下降(P<0.01),四逆汤组与模型组1、2、3h时间段均明显升高,6h明显下降(P<0.05或P<0.01)。结论:四逆汤对内毒素休克大鼠脑损伤具有明显的保护效应,其机制可能是通过抑制促炎性细胞因子TNF-α和促进自由基清除剂SOD的合成,从而拮抗过度的全身性炎性反应而实现的。
OBJECTIVE: To investigate the regular changes of tumor necrosis factor-α (TNF-α) and superoxide dismutase (SOD) contents in brain tissue of endotoxin-shocked rats with endotoxic shock brain injury as the starting point. The central process of microcirculatory disturbance during shock provides a new way for emergency treatment technology. METHODS: A total of 72 6-8 week-old SD rats weighing 180-200 g were randomly divided into sham operation group, model group and SND group, 24 rats in each group. A rat model of endotoxin shock was established. The content of TNF-α in brain tissue was determined by ELISA. Quantitative determination of SOD was performed by spectrophotometry. The TNF-α at 1, 2, 3, and 6 h of brain tissue in each group was detected and analyzed. And SOD content. RESULTS: 1 After endotoxin shock, the content of TNF-α in brain tissue of model group peaked at 6h, and the time of model group was significantly higher than that of sham group (P<0.01). Sini Decoction group and model group The period of 3 and 6 hours decreased significantly (P<0.05 or P<0.01). 2 After SOD shock, SOD content in brain tissue of model group peaked at 6h, and the time of model group was significantly decreased compared with sham group (P<0.01). Sini Decoction group and model group 1, 2 and 3h The time period was significantly increased and significantly decreased at 6h (P<0.05 or P<0.01). Conclusion: Sini decoction has obvious protective effect on brain injury in rats with endotoxin shock. The mechanism may be to antagonize excessive systemic inflammation by inhibiting the synthesis of pro-inflammatory cytokine TNF-α and promoting the synthesis of free radical scavenger SOD. Sexual responses are achieved.