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机构地区:[1]河南科技大学第一附属医院神经外科,洛阳471003
出 处:《现代预防医学》2009年第12期2348-2349,共2页Modern Preventive Medicine
摘 要:[目的]观察氯胺酮对颅脑损伤大鼠血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)及神经细胞凋亡的影响。[方法]实验共分3大组:伪手术组、损伤模型组、氯胺酮治疗组,后两组再根据取材时间分24h、72h、168h组。应用改良的Feeney自由落体法建立颅脑损伤模型,伪手术组只开骨窗,不打击致伤,治疗组造模方法与模型组相同,伤后1h腹腔注射氯胺酮120mg/kg,每隔12h加用1次,在规定时间取血清,检测TNF-α、IL-6含量;取损伤部位脑组织固定、包埋、切片,免疫组化法观察细胞凋亡。[结果]模型建立后,大鼠血清中TNF-α、IL-6含量明显升高,神经细胞凋亡明显增加,用氯胺酮治疗,能明显抑制血清中TNF-α、IL-6的升高和神经细胞凋亡的增加。[结论]氯胺酮能够抑制颅脑损伤大鼠血清TNF-α、IL-6的升高和凋亡细胞过表达,对颅脑损伤具有保护作用。[Objective] To observe the effect of ketamine on the serum levels of TNF-α, IL-6 and the neuronal apoptosis in rats with trmatic brain injury (TBI). [Methods] Sixty-three healthy male rats were randomly divided into three groups: sham operation group, TBI model group and ketamine treatment group. TBI model group and ketamine treatment group were divided into 24, 72, 168 hours groups. The sham operation group only received scalp discussion and sphenotresia, the TBI roodels were established by modified Feeneys Free-falling Weight on the exposed dura, and the ketamine treatment group received 120mg/kg of ketamine through intraperitoneally per 12 hours. The serum levels of TNF-α and IL-6 in each group were determined by ELISA methods, the neuronal apoptosis was observed by immunohistochemieal method. [ Results] The expression of TNF-α and IL-6 in TBI model group were significantly higher than that in sham-operation group (P 〈 0.05) , and treatment with ketalnine conld led to a significant decrease of TNF-α and IL-6 in serum compared with the TBI model (P 〈 0.05). Meanwhile, compared with TBI model group, neuronal apoptosis were significantly inhibited in damaged brain tissue in the treatment group (P 〈 0.05). [ Conclusion] Ketamine showed potential protectiveness on the rats with TBI through inhibiting the over-expression of TNF-α and IL-6 in serum and neuronal apoptosis.
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