关附甲素抗氧化和抗房颤作用

研究关附甲素(Guanfu base A,GFA)的抗房颤和抗氧化作用。大鼠尾静脉注射乙酰胆碱-氯化钙混合液(Ca Cl210 mg/m L,Ach 66μg/m L),连续7 d建立房颤模型。SD大鼠分为正常组、模型组、GFA治疗组(6 mg/kg,12 mg/kg)、胺碘酮(Amiodarone,Ami)治疗组(50 mg/kg)以及洛伐他汀(Lovastatin,Lov)治疗组(10 mg/kg)。测定大鼠房颤持续时间和有效不应期(AERP),用实时荧光定量PCR方法和Western blot方法测定氧化应激相关基因表达,试剂盒测定抗氧化酶的活性。结果显示:与模型组相比,GFA(6 mg/kg,12 mg/kg,po)治疗4 d后能缩短房颤持续时间,延长AERP,超氧化物歧化酶的活力提高,丙二醛含量明显下降。心房肌p22phox、p47phox、p67phox、gp91phox表达下调,膜Rac-1与胞浆Rac-1比值显著下降,缝隙连接蛋白(connexin40)表达升高。提示GFA(6 mg/kg,12 mg/kg)能有效抑制房颤引起的大鼠心房氧化应激损害,抑制房颤发生。     

The effects of aspirin on gastric mucosal integrity, surface hydrophobicity, and prostaglandin metabolism in cyclooxygenase knockout mice

BACKGROUND & AIMS: Insight into the role of the different cyclooxygenase isoforms in prostaglandin biosynthesis, surface hydrophobicity, and gastric mucosal barrier integrity can be gained by comparing the effects of luminal damaging agents in wild-type and cyclooxygenase knockout mice. METHODS: Fasted wild-type, cyclooxygenase-1, and cyclooxygenase-2 knockout mice were intragastrically administered saline, 0.6N HCl, or aspirin (aspirin 20 mmol/L) in combination with 0.6N HCl and killed 1 hour later, at which time the gastric lesion score was assessed and biopsy samples were taken for surface, biochemical, and morphological analyses. RESULTS: The gastric mucosa of cyclooxygenase-1 knockout mice was more severely injured by both HCl alone and aspirin/HCl than that of wild-type and cyclooxygenase-2 knockout mice. HCl alone and aspirin/HCl also induced a more profound decrease in surface hydrophobicity in cyclooxygenase-1 knockout mice than in wild-type mice, whereas this surface property was unaffected in cyclooxygenase-2 knockout mice. The gastric injury induced by aspirin/HCl in cyclooxygenase-1 knockout mice could be prevented if the animals were treated with phosphatidylcholine-associated aspirin. Aspirin/HCl, in comparison to saline or HCl alone, induced a 4-6-fold increase in gastric mucosal prostaglandin E(2) concentration in the cyclooxygenase-1 knockout mice, whereas it decreased prostaglandin E(2) levels in wild-type and cyclooxygenase-2 knockout mice. This paradoxical aspirin-induced increase in gastric prostaglandin E(2) in cyclooxygenase-1 knockout mice seemed to correspond to an increase in cyclooxygenase-2 messenger RNA and protein expression. The gastric lesion score seemed to be significantly associated with alterations in surface hydrophobicity but not with mucosal prostaglandin E(2) concentration. CONCLUSIONS: Our evidence on cyclooxygenase knockout mice suggests that aspirin predominantly causes gastric injury by a non-prostaglandin mechanism, perhaps by attenuating surface hydrophobicity, a possibility supported by the low gastric toxicity of phosphatidylcholine/aspirin. However, prostaglandins generated by cyclooxygenase-1 may play an important permissive role in maintaining gastric mucosal barrier integrity. Aspirin seems to paradoxically increase the gastric mucosal prostaglandin E(2) concentration in cyclooxygenase-1 knockout mice, possibly by the induction of cyclooxygenase-2.     

口腔贱金属合金修复体的生物相容性试验

贱金属合金烤瓷熔附金属修复体是口腔临床修复体应用的主体,存在着较高的不安全性,其生物相容性评价主要有细胞毒性试验、动物试验和临床前试验.细胞毒性检测主要有中性红试验、51Cr释放法、分子滤过试验、甲噻唑四唑氮比色试验、细胞计数试剂盒8试验、乳酸脱氢酶试验、红细胞溶血试验和流式细胞计数等,使用最广泛的细胞是L929细胞和海拉细胞.按细胞接触方式的不同,毒性试验细胞的培养分为浸提液培养法、直接接触法和间接接触法.动物试验可从整体上评价生物相容性,可产生免疫或补体激活反应,但试验难以控制,费用高,费时.动物试验可弥补细胞毒性试验难以模拟的综合反应,因此其与细胞毒性试验一样都是口腔材料生物相容性评价必不可少的环节.