Álefe Brito Monteiro , Humberto Hugo Nunes de Andrade , Erika da Cruz Guedes , Anne Caroline Ribeiro Portela , Hugo Fernandes Oliveira Pires , Maria Janice Pereira Lopes , Nayana Maria Medeiros Vilar Barbosa , Adriano Francisco Alves , Adriana Maria Fernandes de Oliveira Golzio , Damião Pergentino de Sousa , Cícero Francisco Bezerra Felipe , Reinaldo Nóbrega de Almeida
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The administration of CA (50–200 mg/kg, i.p., 30 min prior to PTZ and 0.7–25 mg/kg, i.p., 60 min prior to PTZ) increased the latency to seizure onset and the latency to death. The effects observed with CA treatment at 60 min were partially reversed by pretreatment with flumazenil. Furthermore, neurochemical assays indicated that CA reduced the concentration of malondialdehyde and nitrite, while increasing the concentration of reduced glutathione. Finally, histomorphometric and immunohistochemistry analysis revealed a reduction in inflammation and an increase in neuronal preservation in the hippocampi of CA pre-treated mice. Taken together, the results suggest that CA seems to modulate the GABAA receptor, decrease oxidative stress, mitigate neuroinflammation, and reduce cell death processes.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"179 ","pages":"Article 105807"},"PeriodicalIF":4.4000,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Neuroprotective effect of cinnamic alcohol: A bioactive compound of Cinnamomum spp. essential oil\",\"authors\":\"Álefe Brito Monteiro , Humberto Hugo Nunes de Andrade , Erika da Cruz Guedes , Anne Caroline Ribeiro Portela , Hugo Fernandes Oliveira Pires , Maria Janice Pereira Lopes , Nayana Maria Medeiros Vilar Barbosa , Adriano Francisco Alves , Adriana Maria Fernandes de Oliveira Golzio , Damião Pergentino de Sousa , Cícero Francisco Bezerra Felipe , Reinaldo Nóbrega de Almeida\",\"doi\":\"10.1016/j.neuint.2024.105807\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Cinnamic alcohol (CA) is a phenylpropanoid found in the essential oil of the bark of the genus <em>Cinnamomum</em> spp. Schaeff. 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引用次数: 0
摘要
肉桂醇(CA)是肉桂属(Cinnamomum spp.(Lauraceae Juss.)树皮的精油中发现的一种苯丙酮类化合物。评估 CA 对戊烯四唑(PTZ)诱导的癫痫发作模型小鼠的神经保护作用及其可能的作用机制。研究人员对小鼠进行了行为、神经化学、组织形态学和免疫组化分析。CA(50 - 200 mg/kg, i.p., 30 minutes before PTZ and 0.7 - 25 mg/kg, i.p., 60 minutes before PTZ)能延长癫痫发作的潜伏期和死亡潜伏期。使用氟马西尼预处理可部分逆转60分钟CA处理观察到的效应。此外,神经化学分析表明,CA 降低了丙二醛和亚硝酸盐的浓度,同时增加了还原型谷胱甘肽的浓度。最后,组织形态计量学和免疫组化分析表明,CA 预处理小鼠的海马中炎症减少,神经元保存增加。综上所述,研究结果表明,CA 似乎可以调节 GABAA 受体、降低氧化应激、减轻神经炎症和减少细胞死亡过程。
Neuroprotective effect of cinnamic alcohol: A bioactive compound of Cinnamomum spp. essential oil
Cinnamic alcohol (CA) is a phenylpropanoid found in the essential oil of the bark of the genus Cinnamomum spp. Schaeff. (Lauraceae Juss.), known as cinnamon. To evaluate the neuroprotective effect of CA and its possible mechanism of action on mice submitted to the pentylenetetrazole (PTZ) induced epileptic seizures model. Behavioral, neurochemical, histomorphometric and immunohistochemistry analysis were carried out. The administration of CA (50–200 mg/kg, i.p., 30 min prior to PTZ and 0.7–25 mg/kg, i.p., 60 min prior to PTZ) increased the latency to seizure onset and the latency to death. The effects observed with CA treatment at 60 min were partially reversed by pretreatment with flumazenil. Furthermore, neurochemical assays indicated that CA reduced the concentration of malondialdehyde and nitrite, while increasing the concentration of reduced glutathione. Finally, histomorphometric and immunohistochemistry analysis revealed a reduction in inflammation and an increase in neuronal preservation in the hippocampi of CA pre-treated mice. Taken together, the results suggest that CA seems to modulate the GABAA receptor, decrease oxidative stress, mitigate neuroinflammation, and reduce cell death processes.
期刊介绍:
Neurochemistry International is devoted to the rapid publication of outstanding original articles and timely reviews in neurochemistry. Manuscripts on a broad range of topics will be considered, including molecular and cellular neurochemistry, neuropharmacology and genetic aspects of CNS function, neuroimmunology, metabolism as well as the neurochemistry of neurological and psychiatric disorders of the CNS.