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在戊四氮诱导的癫痫小鼠模型中的神经保护作用。 （你提供的原文不完整，“of”后面缺少具体内容）

Neuroprotective effects of in a mouse model of pentylenetetrazole-induced seizures.

作者信息

Mansouri Somaieh, Hosseini Mahmoud, Beheshti Farimah, Sobhanifar Mohammad-Ali, Rakhshandeh Hassan, Anaeigoudari Akbar

机构信息

Pharmacological Research Center of Medicinal Plants, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

Department of Anatomy, School of Medicine, North Khorasan University of Medical Sciences, Bojnurd, Iran.

出版信息

Avicenna J Phytomed. 2021 Nov-Dec;11(6):610-621. doi: 10.22038/AJP.2021.18562.

DOI:10.22038/AJP.2021.18562
PMID:34804898
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8588953/
Abstract

OBJECTIVE

Oxidative stress has pernicious effects on the brain. has antioxidant properties. We explored neuroprotective effect of against pentylenetetrazole (PTZ)-induced seizures.

MATERIALS AND METHODS

Male mice (BALB/c) were grouped as control, PTZ, Soxhlet (Sox) 100, Sox 200, Macerated (Mac) 100 and Mac 200 groups. Sox and Mac extracts (100 and 200 mg/kg) were injected during 7 days. Delay in onset of minimal clonic seizure (MCS) and generalized tonic- clonic seizure (GTCS) was measured. Number of dark neurons (DN) and levels of oxidative stress indicators in the hippocampus were evaluated.

RESULTS

Onset of MCS and GTCS was later in groups treated with the extracts than the PTZ group (p<0.01 and p<0.001). Number of DN in the hippocampus in the PTZ group was higher than the control group (p<0.001) while in the extract groups, was lower than the PTZ group (p<0.05, p<0.01 and p<0.001). MDA level was higher whereas total thiol level and activity of SOD and CAT were lower (p<0.001) in the PTZ group than the control group. MDA level in the Sox 100 (p<0.01), Sox 200 (p<0.001) and Mac 200 (p<0.01) groups was less than the PTZ group. Total thiol level in the Sox 200 (p<0.001), SOD in the Sox 100 (p<0.05), Sox 200, and Mac 200 and CAT in the Sox 200 (p<0.001) groups were higher than the PTZ group.

CONCLUSION

prevented neuronal death and reduced seizures caused by PTZ via improving brain oxidative stress.

摘要

目的

氧化应激对大脑有有害影响。具有抗氧化特性。我们探讨了其对戊四氮（PTZ）诱导的癫痫发作的神经保护作用。

材料与方法

将雄性小鼠（BALB/c）分为对照组、PTZ组、索氏提取法（Sox）100组、Sox 200组、浸渍法（Mac）100组和Mac 200组。在7天内注射Sox和Mac提取物（100和200mg/kg）。测量最小阵挛性发作（MCS）和全身强直阵挛性发作（GTCS）发作的延迟时间。评估海马中暗神经元（DN）的数量和氧化应激指标水平。

结果

提取物处理组的MCS和GTCS发作时间比PTZ组晚（p<0.01和p<0.001）。PTZ组海马中DN的数量高于对照组（p<0.001），而提取物组低于PTZ组（p<0.05、p<0.01和p<0.001）。PTZ组的丙二醛（MDA）水平较高，而总巯基水平以及超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性较低（p<0.001）。Sox 100组（p<0.01）、Sox 200组（p<0.001）和Mac 200组（p<0.01）的MDA水平低于PTZ组。Sox 200组的总巯基水平（p<0.001）、Sox 100组（p<0.05）、Sox 200组和Mac 200组的SOD以及Sox 200组的CAT高于PTZ组。

结论

通过改善脑氧化应激，预防了PTZ引起的神经元死亡并减少了癫痫发作。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6f6/8588953/4c0155113118/AJP-11-610-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6f6/8588953/4f5bc7f449a4/AJP-11-610-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6f6/8588953/4909d3092b4c/AJP-11-610-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6f6/8588953/4b4250f7c36c/AJP-11-610-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6f6/8588953/ce1ded5cf09d/AJP-11-610-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6f6/8588953/3031cd6c45b3/AJP-11-610-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6f6/8588953/12604b60dc72/AJP-11-610-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6f6/8588953/4c0155113118/AJP-11-610-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6f6/8588953/4f5bc7f449a4/AJP-11-610-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6f6/8588953/4909d3092b4c/AJP-11-610-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6f6/8588953/4b4250f7c36c/AJP-11-610-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6f6/8588953/ce1ded5cf09d/AJP-11-610-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6f6/8588953/3031cd6c45b3/AJP-11-610-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6f6/8588953/12604b60dc72/AJP-11-610-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6f6/8588953/4c0155113118/AJP-11-610-g007.jpg

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