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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Piperine decreases pilocarpine-induced convulsions by GABAergic mechanisms.
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Piperine decreases pilocarpine-induced convulsions by GABAergic mechanisms.

机译：Piperine通过Gabaergic机制降低了汲昆宾诱导的痉挛。

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Piperine, an alkaloid present in the Piper genus, was shown to have an anticonvulsant activity, evaluated by the pilocarpine-induced model, in mice. Pilocarpine (350mg/kg, i.p.) was administered 30min after piperine (2.5, 5, 10 and 20mg/kg, i.p.) which significantly increased latencies to 1st convulsion and to death, and percentage of survivals. These parameters were also increased in the pilocarpine groups pretreated with atropine plus piperine (10 and 2.5mg/kg, respectively), as related to the pilocarpine group. However, they were not altered in the pilocarpine groups pretreated with memantine (a NMDA-type glutamate receptors blocker, 2mg/kg, p.o.) or nimodipine (a calcium channel blocker, 10mg/kg, p.o.), both associated with piperine (1 or 2.5mg/kg), as compared to the piperine plus pilocarpine group. Moreover, the pilocarpine group pretreated with diazepam (which binds to the GABAA receptor, 0.2 and 0.5mg/kg, i.p.) plus piperine (1 and 2.5mg/kg) significantly increased latency to the 1st convulsion, as related to the pilocarpine group, suggesting that the GABAergic system is involved with the piperine action. Furthermore, the piperine effect was blocked by flumazenil (2mg/kg, i.p.), a benzodiazepine antagonist. Untreated P350 animals showed decreased striatal DA and increased DOPAC and HVA levels that were not affected in the piperine plus pilocarpine groups. Piperine increased striatal levels of GABA, glycine and taurine, and reversed pilocarpine-induced increases in nitrite contents in sera and brain. Hippocampi from the untreated pilocarpine group showed an increased number of TNF-α immunostained cells in all areas, as opposed to the pilocarpine group pretreated with piperine. Taken together, piperine anticonvulsant effects are the result of its anti-inflammatory and antioxidant actions, as well as TNF-α reduction. In addition, piperine effects on inhibitory amino acids and on the GABAergic system may certainly contribute to the drug anticonvulsant activity.
机译：哌啶，存在于吹笛子属中的生物碱，被示出具有抗惊厥活性，由小鼠中汲昆宾诱导的模型评估。哌啶（350mg / kg，i.p.）哌啶（2.5,5,10和20mg / kg，i.p.）施用30min，其显着增加了延迟，延迟了延迟和死亡，以及幸存者的百分比。在与柳甘油基团的阿托品加哌啶（10和2.5mg / kg）预处理的紫罗兰甘石基团中也增加了这些参数。然而，它们没有改变用Memantine（NMDA型谷氨酸受体阻滞剂，2mg / kg，PO）或奈代峰（钙通道阻断剂，10mg / kg，PO），嗜哌啶（NMDA型谷氨酸受体阻滞剂，2mg / kg，po），两者与哌啶相关（1或与哌啶加毒素组相比，2.5mg / kg。此外，用二嗪泮预处理的柳甘油基团（与GABAA受体结合，0.2和0.2和0.5mg / kg，IP）加上哌啶（1和2.5mg / kg）显着增加了第一个惊厥的潜伏期，如柳甘油群组织，表明加布枸杞系统涉及哌啶作用。此外，哌嗪菌（2mg / kg，I.p.）阻断哌嗪效应，苯二氮卓肝拮抗剂。未处理的P350动物表明，哌啶和哌啶加毒素组不受影响的偏纹玻璃鳞和增加的多奥多卡和HVA水平。哌啶增加了GABA，甘氨酸和牛磺酸的纹状体水平，血清和脑中的亚硝酸盐含量的逆转的紫罗兰甘油诱导的增加。来自未处理的汲取杀野组的海马在所有区域中显示出含有预处理的柳甘油基团的TNF-α免疫染色细胞数量增加。连合在一起，哌啶抗惊厥作用是其抗炎和抗氧化作用的结果，以及TNF-α还原。此外，对抑制氨基酸和加巴生物系统的哌啶作用可能肯定有助于药物抗惊厥活性。

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