罗哌卡因与布比卡因对兔缺血 再灌注心肌c fos基因表达的影响

目的：研究布比卡因、罗哌卡因对心肌缺血 再灌注的影响，从分子水平研究两者的心脏毒性。方法：大白兔40只，随机分为4组各10只：①对照组(N组)；②心肌缺血30 min再灌注30 min组(IR组)；③布比卡因组(BUP组)：心肌缺血30 min再灌注布比卡因1 μg·mL 1 10 min。④罗哌卡因组(ROP组)：心肌缺血30 min再灌注罗哌卡因1 μg·mL 1 10 min。应用Langendorff缺血 再灌注模型，提取大白兔心肌总RNA与经同位素标记的 c fos cDNA探针进行分子杂交并自显影，测定c fos基因mRNA水平。结果：N、IR、ROP、BUP组心肌c fos基因mRNA杂交点吸光度值分别为1.842±0.063，11.855±1.257，18.736±1.875，59.647±2.336。ROP、BUP组心肌缺血 再灌注时 c fos基因的表达均显著增加(均P＜0.01)。结论：c fos基因可能参与了心肌缺血 再灌注过程。布比卡因、罗哌卡因的心脏毒性作用可能与c fos基因有关。罗哌卡因的心脏毒性小于布比卡因。     

植物雌激素对去势雌大鼠缺血脑组织C-fos表达的影响

目的：对比研究哺乳动物雌激素和植物雌激素对大鼠局灶性脑缺血后脑组织C-fos表达的影响．方法：将90只雌性去势SD大鼠随机分成空白对照组，雌激素组和葛根素组，每组30只．所有大鼠均制作成右侧永久性大脑中动脉阻断模型．采用免疫组化方法检测去势雌性大鼠脑缺血后不同时间点脑组织C-fos的表达．结果：雌激素组和葛根素组大鼠脑缺血后脑组织C—fos的表达均下降，发生作用的时间段在脑缺血后16h至24h．在脑缺血后8h，3组表达C-fos的阳性细胞数无统计学差异．在16h及24h时间点，用药组与对照组相比，C—fos阳性细胞数明显减少（P〈0．05）；用药组之间相比无统计学意义（P〉0．05）．结论：两种雌激素均能减弱脑缺血后脑组织C—fos的表达．     

P16和C-fos在子宫平滑肌肿瘤中的表达及意义

目的:探讨抑癌基因P16和原癌基因C-fos在子宫平滑肌瘤和子宫平滑肌肉瘤中的表达.方法:采用免疫组织化学SP法对40例子宫平滑肌瘤、10例子宫平滑肌肉瘤和20例正常子宫平滑肌进行P16和C-fos基因蛋白检测.结果:P16基因蛋白在子宫平滑肌肉瘤中的表达率显著高于子宫平滑肌瘤和正常子宫平滑肌组(P＜0.05),其在子宫平滑肌瘤中的表达率亦高于正常子宫平滑肌组(P＜0.05);C-fos基因蛋白在子宫平滑肌肉瘤中的表达率显著高于子宫平滑肌瘤和正常子宫平滑肌组(P＜0.05),但其在子宫平滑肌瘤和正常子宫平滑肌组间的表达没有明显区别(P＞0.05).结论:P16和C-fos的表达可能和子宫平滑肌瘤向子宫平滑肌肉瘤的转化密切相关;其为临床鉴别子宫平滑肌肿瘤良恶性提供参考.     

康欣胶囊及其拆方对肾虚血瘀型大鼠神经细胞的保护作用

目的探讨康欣胶囊全方及其补肾、健脾、养血活血3组拆方对肾虚血瘀型血管性痴呆（VD）大鼠神经细胞的影响。方法采用双侧椎动脉永久性封闭和摘除单侧性器官建立肾虚血瘀型VD模型大鼠,分别给予康欣胶囊全方（全方组）、康欣胶囊补肾方（补肾组）、康欣胶囊健脾方（健脾组）、康欣胶囊养血活血方（养血活血组）、阳性对照药喜得镇（西药组）和蒸馏水（模型组）。结果全方组大鼠空间探索能力显著优于其他组（P〈0.01）;全方组海马神经细胞器及细胞核固缩情况轻于其他各组;全方组能增加海马乙酰胆碱含量（P〈0.01）,提高VD大鼠海马酪氨酸激酶A、核转录因子、原癌基因C-fos、神经生长因子受体的表达（P〈0.01）,降低胶质纤维酸性蛋白的表达（P〈0.05）。结论康欣胶囊全方对肾虚血瘀型血管性痴呆大鼠神经细胞具有保护作用。     

Preemptive effect of intravenous ketamine in the rat: concordance between pain behavior and spinal fos-like immunoreactivity

BACKGROUND: The purpose of this study was to compare behavioral antinociceptive responses with spinal fos-like immunoreactivity (FLI) for a intravenous ketamine injection between pre vs. postformalin administration in rats. METHODS: Sprague-Dawley rats (250-300 g) were prepared to receive either saline or ketamine. All rats were randomly divided into three groups: control, pretreatment and post-treatment group. Formalin (5%) 100 microl was injected into the hindpaw. Pain related behavior and FLI in the lumbar spinal cord was examined. RESULTS: Flinches of phase 2 were 239.3 (22,8), 118.6 (7,5) (P < 0.05 vs. control and post-treatment group), and 186.7 (16,6) in the control, pre and, post-treatment groups, respectively. Fos-like immunoreactivity expression was significantly correlated with phase 2 flinching behavior (P < 0.001). CONCLUSION: Pretreatment with intravenous ketamine inhibits inflammatory pain behavior and FLI expression following a formalin injection in rats, suggesting that pretreatment of ketamine plays an important role in preemptive analgesia.     

Regional differences in naloxone modulation of Delta(9)-THC induced Fos expression in rat brain

Recent behavioral and pharmacological research shows extensive interplay between cannabinoid and opioid neurochemical systems. Here we examined the neuroanatomical basis of this interaction using c-fos immunohistochemistry. We compared Fos immunoreactivity in groups of male albino Wistar rats treated with vehicle, Delta(9)-tetrahydrocannabinol (THC, 10 mg/kg, i.p.), naloxone (10 mg/kg, i.p.) or THC and naloxone in combination. Locomotor activity was depressed in both THC treatment groups and moderately inhibited in rats given naloxone alone. Results showed that naloxone inhibited THC-induced Fos immunoreactivity in several key brain regions including the ventral tegmental area, ventromedial and dorsomedial hypothalamus, central caudate-putamen and ventrolateral periaqueductal grey. Conversely, naloxone and THC had an additive effect on Fos immunoreactivity in the central nucleus of the amygdala, the bed nucleus of the stria terminalis (lateral division), the insular cortex, and the paraventricular nucleus of the thalamus. These findings complement earlier pharmacological results showing potent modulation of cannabinoid-induced analgesia, appetite and reward by opioids. The inhibitory effects of naloxone on THC-induced ventral tegmentum, hypothalamic and periaqueductal grey Fos expression point to these structures as key sites involved in cannabinoid-opioid interactions.     

芝麻素对肾性高血压伴高血脂大鼠心肌肥厚的影响

目的:探讨芝麻素对肾性高血压伴高血脂大鼠(RHHR)心肌肥厚的影响。方法:RHHR灌服不同剂量芝麻素(100,33,10mg·kg^-1·d^-1)8周后处死动物,计算左室重量指数(LVWI);测定心肌羟脯氨酸(HYD)和硝酸盐/亚硝酸盐(NO^-₃/NO^-₂)含量;免疫组化法观察心肌C-fos蛋白表达;透射电镜观察心肌超微结构。结果:100mg.kg^-1芝麻素明显降低心肌LVWI,HYD含量和C-fos蛋白表达,升高NO^-₃/NO^-₂浓度,改善肌丝排列紊乱,胶原纤维增生等病理变化。结论:芝麻素逆转RHHR心肌肥厚的机制可能与恢复NO水平,降低C-fos蛋白表达有关。     

Hippocampal involvement in the expression of kindling-induced fear in rats

Kindling dramatically increases fearful behavior in rats. Because kindling-induced fear increases in magnitude as rats receive more stimulations, kindling provides a superb opportunity to study the nature and neural mechanisms of fear sensitization. Interestingly, these changes in behavior are accompanied by increased binding to inhibitory receptors and decreased binding to excitatory receptors in the CA1 and dentate gyrus regions of the hippocampus. This led us to hypothesize that kindling-induced fear may result from an increased inhibitory tone within hippocampal circuits. To test this hypothesis, we investigated FOS protein immunoreactivity in hippocampal and amygdalar regions of kindled rats that were exposed to an unfamiliar open field. We found that FOS immunoreactivity was significantly decreased in the CA1 region, dentate gyrus, and perirhinal cortex of kindled rats compared to sham-stimulated rats. These results support our hypothesis that kindling-induced fear may be produced by inhibition within hippocampal circuits. They also suggest that neural changes within the hippocampus may be important for the sensitization of fear.     

鞘内注射昂丹司琼对慢性脊神经炎性痛大鼠的影响

目的探讨鞘内给予5-HT3受体阻滞剂昂丹司琼对慢性脊神经炎性痛大鼠行为学及脊髓背角c-Fos蛋白表达的影响。方法成年雄性SD大鼠48只随机均分为6组（n=8）：空白组（A组）、模型组（B组）、生理盐水组（C组）和昂丹司琼10μg/kg组（D1组）、25μg/kg组（D2组）、50μg/kg组（D3组）。制作大鼠脊神经炎性痛模型后14 d行鞘内注射,并测定大鼠机械缩足反射阈值和热缩足反射潜伏期的变化情况;应用免疫组化技术观察大鼠脊髓c-Fos表达变化情况。结果与B组相比,D2组机械缩足反射阈值、热缩足反射潜伏期明显增高、脊髓背角中c-Fos蛋白表达显著减少（P〈0.01）,D1组与B组比较,无明显变化（P〉0.05）;D2与D3组间差异无统计学意义（P〉0.05）。结论鞘内给予昂丹司琼25μg/kg可以减轻大鼠慢性脊神经炎性痛导致的痛觉过敏。     

神经生长因子通过c-fos促进支气管上皮细胞NK-1R表达

目的探讨神经生长因子(NGF)通过c-fos影响支气管上皮细胞NK-1R的表达。方法以人支气管上皮细胞(NHBEC)为研究对象,通过阳离子脂质体将c-fos siRNA转染至细胞内,然后用NGF干预。实验设五组:对照组、NGF干预组、NGF+c-fos siRNA组、NGF+空白脂质体组、NGF+非特异性dsRNA组。转染12 h后,用NGF干预60 min,采用Western blot法测定c-fos蛋白表达,采用免疫细胞化学法和RT-PCR从蛋白和mRNA水平观察细胞中NK-1R的表达。结果与对照组比,NGF组c-fos蛋白、NK-1R蛋白和NK-1RmRNA表达均明显增加(P0.01);与NGF组比,NGF+c-fos siRNA组中c-fos蛋白、NK-1R蛋白和NK-1RmRNA表达均明显减少(P0.01),而NGF组、NGF+空白脂质体组、NGF+非特异性dsRNA组之间的c-fos蛋白、NK-1R蛋白和NK-1RmRNA表达无显著差异。结论 NGF可通过c-fos促进支气管上皮细胞中NK-1R的表达,介导哮喘神经源性炎症,RNAi技术可以减少NGF诱导的人支气管上皮细胞c-fos蛋白及NK-1R的表达。