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目的 :研究吗啡依赖及戒断状态下嘌呤核苷酸分解代谢的变化及作用机制。方法 :剂量递增腹腔注射盐酸吗啡 ,建立吗啡依赖及戒断大鼠模型。试剂盒检测血浆尿酸含量、血浆及小肠组织黄嘌呤氧化酶 (XO)的活性。提取小肠组织总 RNA,采用逆转录聚合酶链反应 (RT- PCR)检测小肠组织 XO m RNA的水平 ,以 β- actinm RNA为内标。结果 :血浆尿酸水平显示 ,7d吗啡用药组明显高于对照组 (P<0 .0 5 ) ;血浆 XO酶学结果显示 ,7d吗啡用药组 XO明显高于对照组 (P<0 .0 5 ) ,自然戒断组与纳洛酮对照组也明显高于对照组 (P<0 .0 1 ) ;小肠组织 XO酶学结果可见 ,7d吗啡用药组与纳洛酮戒断组 XO明显高于对照组 (P<0 .0 5 ) ;小肠组织 XO的 m RNA水平可见 ,7d吗啡用药组、自然戒断组和纳洛酮戒断组 XO m RNA水平明显高于对照组。结论 :吗啡促进嘌呤核苷酸分解代谢 ;吗啡促进大鼠小肠嘌呤核苷酸分解代谢关键酶 XO的活性 ,纳洛酮不能阻断该作用。提示吗啡对小肠 XO的作用是通过非 μ受体途径
Objective: To study the changes and mechanisms of purine nucleoside catabolism in morphine dependent and withdrawal states. Methods: Morphine hydrochloride was administered intraperitoneally to rats in dose-dependent manner. Morphine dependence and withdrawal models were established. Kits were tested for uric acid, xanthine oxidase (XO) activity in plasma and small intestine. Total RNA was extracted from small intestine, and the level of XO m RNA in small intestine was detected by RT-PCR. Β-actin mRNA was used as internal standard. Results: The levels of plasma uric acid in the morphine group at 7d were significantly higher than those in the control group (P <0.05). The plasma XO enzymatic results showed that the XO of the morphine group at 7d was significantly higher than that of the control group (P <0.05) , And the natural withdrawal group and naloxone control group were also significantly higher than the control group (P <0 01); XO enzymatic results of small intestine, morphine treatment group and naloxone withdrawal group 7d was significantly higher than the control (P <0.05). The level of m RNA in XO of small intestine was visible. The levels of XO m RNA in morphine treated group, natural withdrawal group and naloxone withdrawal group were significantly higher than those in control group. CONCLUSION: Morphine promotes purine nucleotide catabolism. Morphine enhances the activity of XO, a key enzyme of purine nucleotide catabolism in rats. Naloxone can not block this effect. Suggesting that the effect of morphine on small intestine XO is through the non-mu receptor pathway