强痛宁对大鼠中枢脑区NO/cGMP信号转导通路影响

Effects of the QIANG TONG NING on NO/cGMP Signal Pathway in in the Central Brain Regions of Rats

为了研究强痛宁麻醉下大鼠中枢脑区一氧化碳合酶(NOS)活性、NO和环乌苷酸(cGMP)浓度变化,探讨强痛宁麻醉镇痛的中枢作用机理。将24只SD大鼠随机分成4组,分别为对照组、诱导期、麻醉期和催醒期组,于不同时期采集大鼠大脑皮质、小脑、脑干、海马和丘脑。采用比色法测定NOS活性和NO含量,酶联免疫吸附法测定cGMP浓度。结果表明,腹腔注射强痛宁6 mg/kg体重后,麻醉期各脑区NOS活性显著降低(P<0.05或P<0.01);NO产量与对照组比较降低极显著(P<0.01);cGMP浓度降低显著(P<0.05或P<0.01)。结果提示,强痛宁抑制大鼠中枢脑区NOS活性,阻断NO/cGMP信号转导可能是其产生全麻作用的重要机理之一。

The experiment was conducted to investigate the possible molecular mechanisms of QIANG TONG NING（QTN） anesthesia on the central nervous system by analyzing the NOS activity,NO and cGMP contents in central brain regions in rats.Twenty-four SD rats were divided randomly into control group,induction group,anesthesia group,and recovery from anesthesia group.Rat brain samples of cerebral cortex,hippocampus,cerebellum,thalamus and brain stem were separated in different period under specificity anesthetic for deer anesthesia.The activity of NOS and concentration of NO were measured using colorimetry,and cGMP was determined by Elisa.The results showed that the NOS activity was significantly decreased（P〈0.05 or P〈0.01）,the NO contents were significantly decreased（P〈0.01）,and the concentration of cGMP were also obviously decreased（P〈0.05 or P〈0.01）in all encephalic regions in the anesthesia group as compared with control group.These results indicated that the QTN inhibited NOS activity,and blocked NO/cGMP signal conduction suggesting that effects on NO/cGMP signal transduction may be the important mechanism of general anesthesia.