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自愿进行复杂和有规律的轮式跑步运动对糖尿病大鼠海马中 8-氧鸟嘌呤 DNA 糖基化酶、神经丝蛋白 3B、H2O2 和细胞凋亡水平的影响。

The effects of voluntary complex and regular wheel running exercises on the levels of 8-oxoguanine DNA glycosylase, semaphorin 3B, H2O2, and apoptosis in the hippocampus of diabetic rats.

机构信息

Department of Exercise Physiology, Faculty of Sport Sciences, University of Birjand, Birjand, Iran.

Faculty of Sport Sciences, Department of Exercise Physiology, University of Mazandaran, Babolsar, Iran.

出版信息

Brain Behav. 2021 Mar;11(3):e01988. doi: 10.1002/brb3.1988. Epub 2021 Jan 20.

DOI:10.1002/brb3.1988
PMID:33471970
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7994679/
Abstract

PURPOSE

One of the most frequent complications associated with diabetes mellitus is apoptosis within the brain which can lead to cognitive disorders. Exercise is considered the best non-pharmacological approach to reduce the severity and extent of cell death through poorly-understood mechanisms. The aim of this study was to investigate the effects of voluntary complex and regular wheel running on the levels of 8-oxoguanine DNA glycosylase (OGG ), semaphorin 3B (sema3B), hydrogen peroxide (H O ), and apoptosis in the hippocampus of diabetic rats.

METHODS

48 Wistar male rats were randomly divided into 6 groups: healthy control (C), diabetes control (D), regular wheel running + diabetes (RWD), complex wheel running + diabetes (CWD), healthy regular wheel running (RW), and healthy complex wheel running (CW). The diabetic rat model was produced by intraperitoneal injection of streptozotocin (STZ). The protocol encompassed a 4-week voluntary running training regimen on regular and complex wheel running apparatus. The rats were sacrificed 48 hr after the last training session. To measure the protein concentrations within the hippocampus, ELISA has been utilized. One-way ANOVA was used to compare the groups.

RESULTS

There were no significant differences in OGG1 protein levels between the groups. H O level in the D group was significantly higher than the C group (p = .002), while this in RWD and CWD groups was considerably lower than the D group (p = .002 and p = .003, respectively). In the D group, the levels of apoptosis and Sema3B were significantly (p = .001 and p = .007, respectively) higher than C, RWD (p = .001, p = .0001, respectively), and CWD groups (p = .001, p = .006, respectively). Nevertheless, there were not any significant differences between RWD and CWD groups.

CONCLUSION

The increased levels of Sema3B, H2O2, and apoptosis within the hippocampus associated with diabetes could be noticeably restored by both types of voluntary wheel running protocols.

摘要

目的

糖尿病最常见的并发症之一是大脑中的细胞凋亡,这可能导致认知障碍。运动被认为是通过尚未完全了解的机制来降低细胞死亡的严重程度和范围的最佳非药物治疗方法。本研究的目的是研究自愿性复杂和常规轮跑对糖尿病大鼠海马 8-氧鸟嘌呤 DNA 糖基化酶(OGG1)、信号素 3B(sema3B)、过氧化氢(H2O2)和细胞凋亡水平的影响。

方法

将 48 只雄性 Wistar 大鼠随机分为 6 组:健康对照组(C)、糖尿病对照组(D)、常规轮跑+糖尿病组(RWD)、复杂轮跑+糖尿病组(CWD)、健康常规轮跑组(RW)和健康复杂轮跑组(CW)。糖尿病大鼠模型通过腹腔注射链脲佐菌素(STZ)制成。方案包括 4 周的常规和复杂轮跑训练。最后一次训练结束后 48 小时处死大鼠。为了测量海马内的蛋白质浓度,使用了 ELISA。采用单因素方差分析比较各组间的差异。

结果

各组 OGG1 蛋白水平无显著差异。D 组 H2O2 水平明显高于 C 组(p=.002),而 RWD 和 CWD 组明显低于 D 组(p=.002 和 p=.003)。D 组凋亡和 Sema3B 水平明显高于 C、RWD(p=.001 和 p=.007)和 CWD 组(p=.001 和 p=.006)。然而,RWD 和 CWD 组之间没有差异。

结论

糖尿病大鼠海马中 Sema3B、H2O2 和细胞凋亡水平的升高可通过两种自愿轮跑方案明显恢复。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/7994679/e93cc281d056/BRB3-11-e01988-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/7994679/8102933f99f8/BRB3-11-e01988-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/7994679/1be98cd8db05/BRB3-11-e01988-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/7994679/6a91e756116c/BRB3-11-e01988-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/7994679/cb0bf8970bc6/BRB3-11-e01988-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/7994679/e7216219bb55/BRB3-11-e01988-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/7994679/e93cc281d056/BRB3-11-e01988-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/7994679/8102933f99f8/BRB3-11-e01988-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/7994679/1be98cd8db05/BRB3-11-e01988-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/7994679/6a91e756116c/BRB3-11-e01988-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/7994679/cb0bf8970bc6/BRB3-11-e01988-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/7994679/e7216219bb55/BRB3-11-e01988-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/7994679/e93cc281d056/BRB3-11-e01988-g002.jpg

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