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依达拉奉右莰醇可改善多西他赛诱导的大鼠认知障碍:来自生物学行为指标和各向异性分数的证据。

Docetaxel-induced cognitive impairment in rats can be ameliorated by edaravone dexborneol: Evidence from the indicators of biological behavior and anisotropic fraction.

作者信息

Liu Ping, Liu Hai, Wei Lijun, Shi Xun, Wang Wei, Yan Shengxiang, Zhou Wenya, Zhang Jiangong, Han Suxia

机构信息

Department of Radiation Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shanxi, China.

Department of Oncology, Heping Hospital Affiliated to Changzhi Medical College, Changzhi, Shanxi, China.

出版信息

Front Neurosci. 2023 Apr 3;17:1167425. doi: 10.3389/fnins.2023.1167425. eCollection 2023.

DOI:10.3389/fnins.2023.1167425
PMID:37077321
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10106566/
Abstract

OBJECTIVE

This study aimed to investigate the effect of Edaravone Dexborneol (ED) on impaired learning and memory in docetaxel (DTX)-treated rats using cognitive behavior assessments and magnetic resonance diffusion tensor imaging (DTI).

MATERIALS AND METHODS

In total, 24 male Sprague-Dawley rats were divided into control, low-dose DTX (L-DTX) model, and high-dose DTX(H-DTX) model groups, with eight rats in each group, numbered 1-8. The rats were intraperitoneally injected with 1.5 mL of either normal saline (control group), or 3 mg/kg and 6 mg/kg DTX (L-DTX and H-DTX groups, respectively), once a week for 4 weeks. The learning and memory abilities of each group were tested using a water maze. At the end of the water maze test, rats 1-4 in each group were treated with ED (3 mg/kg, 1 mL), and rats 5-8 were injected with an equal volume of normal saline once a day for 2 weeks. The learning and memory abilities of each group were evaluated again using the water maze test, and the image differences in the hippocampus of each group were analyzed using DTI.

RESULTS

(1) H-DTX group (32.33 ± 7.83) had the longest escape latency, followed by the L-DTX group (27.49 ± 7.32), and the Control group (24.52 ± 8.11) having the shortest, with the difference being statistically significant ( < 0.05). (2) Following ED treatment, compared to rats treated with normal saline, the escape latency of the L-DTX (12.00 ± 2.79 vs. 10.77 ± 3.97,  < 0.05), and the H-DTX (12.52 ± 3.69 vs. 9.11 ± 2.88,  < 0.05) rats were significantly shortened. The residence time in the target quadrant of H-DTX rats was significantly prolonged (40.49 ± 5.82 vs. 55.25 ± 6.78,  < 0.05). The CNS damage in the L-DTX rats was repaired to a certain extent during the interval between the two water maze tests (28.89 ± 7.92 vs. 12.00 ± 2.79,  < 0.05). (3) The fractional anisotropy (FA) value of DTI in the hippocampus of rats in the different groups showed variable trends. After treatment with ED, though the FA values of most areas in the hippocampus of rats in L-DTX and H-DTX groups were higher than before, they did not reach the normal level.

CONCLUSION

ED can ameliorate the cognitive dysfunctions caused by DTX in rats by improving the learning and memory impairment, which is reflected in the recovery of biological behavior and DTI indicators of the hippocampus.

摘要

目的

本研究旨在通过认知行为评估和磁共振扩散张量成像(DTI),探讨依达拉奉右莰醇(ED)对多西他赛(DTX)处理的大鼠学习记忆障碍的影响。

材料与方法

将24只雄性Sprague-Dawley大鼠分为对照组、低剂量DTX(L-DTX)模型组和高剂量DTX(H-DTX)模型组,每组8只,编号1-8。大鼠每周腹腔注射1.5 mL生理盐水(对照组)或3 mg/kg和6 mg/kg DTX(分别为L-DTX组和H-DTX组),共4周。每组大鼠的学习和记忆能力通过水迷宫进行测试。在水迷宫测试结束时,每组的1-4号大鼠每天用ED(3 mg/kg,1 mL)处理,5-8号大鼠每天注射等量生理盐水,持续2周。再次使用水迷宫测试评估每组大鼠的学习和记忆能力,并使用DTI分析每组大鼠海马体的图像差异。

结果

(1)H-DTX组(32.33±7.83)的逃避潜伏期最长,其次是L-DTX组(27.49±7.32),对照组(24.52±8.11)最短,差异具有统计学意义(<0.05)。(2)ED处理后,与生理盐水处理的大鼠相比,L-DTX组(12.00±2.79 vs. 10.77±3.97,<0.05)和H-DTX组(12.52±3.69 vs. 9.11±2.88,<0.05)大鼠的逃避潜伏期显著缩短。H-DTX组大鼠在目标象限的停留时间显著延长(40.49±5.82 vs. 55.25±6.78,<0.05)。在两次水迷宫测试的间隔期间,L-DTX组大鼠的中枢神经系统损伤在一定程度上得到修复(28.89±7.92 vs. 12.00±2.79,<0.05)。(3)不同组大鼠海马体DTI的分数各向异性(FA)值呈现不同趋势。ED处理后,虽然L-DTX组和H-DTX组大鼠海马体大部分区域的FA值高于处理前,但未达到正常水平。

结论

ED可通过改善学习记忆障碍来减轻DTX所致大鼠的认知功能障碍,这体现在海马体生物行为和DTI指标的恢复上。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a064/10106566/b4eb03b062e8/fnins-17-1167425-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a064/10106566/a92f2c28ae0e/fnins-17-1167425-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a064/10106566/1f296deedc28/fnins-17-1167425-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a064/10106566/05cca943b3ea/fnins-17-1167425-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a064/10106566/ca71b75ec265/fnins-17-1167425-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a064/10106566/b4eb03b062e8/fnins-17-1167425-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a064/10106566/a92f2c28ae0e/fnins-17-1167425-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a064/10106566/1f296deedc28/fnins-17-1167425-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a064/10106566/0025fc06115b/fnins-17-1167425-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a064/10106566/05cca943b3ea/fnins-17-1167425-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a064/10106566/b4eb03b062e8/fnins-17-1167425-g006.jpg

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