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芍药苷对创伤后应激障碍大鼠模型下丘脑-垂体-肾上腺轴负反馈的调节作用

Paeoniflorin regulates the hypothalamic-pituitary-adrenal axis negative feedback in a rat model of post-traumatic stress disorder.

作者信息

Chen Jie, Ye Weiqiong, Li Ling, Su Junfang, Huang Yunling, Liu Lingyun, Wu Lili, Yan Can

机构信息

The Research Centre of Basic Integrative Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510006, China.

Department of Pathology and Pathophysiology, School of Basic Medical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, China.

出版信息

Iran J Basic Med Sci. 2020 Apr;23(4):439-448. doi: 10.22038/ijbms.2020.41214.9738.

DOI:10.22038/ijbms.2020.41214.9738
PMID:32489558
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7239430/
Abstract

OBJECTIVES

To investigate the effects of paeoniflorin (PEF) on the hypothalamic-pituitary-adrenal (HPA) axis feedback function of post-traumatic stress disorder (PTSD).

MATERIALS AND METHODS

Single-prolonged stress (SPS) was used to establish a PTSD-like rat model. The contents of plasma corticosterone (CORT), adrenocorticotropin hormone (ACTH) and corticotropin-releasing hormone (CRH) were measured by ELISA. Glucocorticoid receptor (GR), mineralocorticoid receptor (MR), adrenocorticotropic hormone-releasing factor I receptor (CRF1R), and adrenocorticotropic hormone-releasing factor II receptor (CRF2R) in the hippocampus and amygdala were measured by RT-PCR and immunohistochemistry.

RESULTS

The results showed that on day 8 after SPS, model rats showed enhanced HPA axis negative feedback lasting to day 29. On day 29, plasma CORT levels increased in model rats, while plasma CRH levels had no significant difference on days 8, 22, and 29. The expression of GR and MR of model rats significantly increased in the hippocampus, while the expression of GR, MR, and CRF1R significantly decreased in the amygdala. After 14 days of continuous administration of PEF, the enhanced negative feedback was inhibited, and the plasma CORT level significantly reduced after 21 days of administration. Moreover, PEF could significantly decrease the expression of GR and MR in the hippocampus, and increase the expression of GR, MR, and CRF1R significantly in the amygdala.

CONCLUSION

PEF could regulate HPA axis dysfunction in a rat model of PTSD, which may be related to regulating expression of GR and MR in the hippocampus and amygdala and regulating expression of CRF1R in the amygdala.

摘要

目的

探讨芍药苷（PEF）对创伤后应激障碍（PTSD）下丘脑-垂体-肾上腺（HPA）轴反馈功能的影响。

材料与方法

采用单次延长应激（SPS）建立PTSD样大鼠模型。采用酶联免疫吸附测定法（ELISA）检测血浆皮质酮（CORT）、促肾上腺皮质激素（ACTH）和促肾上腺皮质激素释放激素（CRH）的含量。采用逆转录-聚合酶链反应（RT-PCR）和免疫组织化学法检测海马和杏仁核中糖皮质激素受体（GR）、盐皮质激素受体（MR）、促肾上腺皮质激素释放因子I受体（CRF1R）和促肾上腺皮质激素释放因子II受体（CRF2R）的表达。

结果

结果显示，SPS后第8天，模型大鼠HPA轴负反馈增强，持续至第29天。第29天，模型大鼠血浆CORT水平升高，而在第8、22和29天血浆CRH水平无显著差异。模型大鼠海马中GR和MR的表达显著增加，而杏仁核中GR、MR和CRF1R的表达显著降低。连续给予PEF 14天后，增强的负反馈被抑制，给药21天后血浆CORT水平显著降低。此外，PEF可显著降低海马中GR和MR的表达，并显著增加杏仁核中GR、MR和CRF1R的表达。

结论

PEF可调节PTSD大鼠模型中的HPA轴功能障碍，这可能与调节海马和杏仁核中GR和MR的表达以及杏仁核中CRF1R的表达有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/64b0b7aa3273/IJBMS-23-439-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/ee449bdb46ba/IJBMS-23-439-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/f4251e92b5ed/IJBMS-23-439-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/87a00df4e2a7/IJBMS-23-439-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/53c0655242b3/IJBMS-23-439-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/5706be176f94/IJBMS-23-439-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/339caad7f376/IJBMS-23-439-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/6118cd590ebf/IJBMS-23-439-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/cca69d9896f9/IJBMS-23-439-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/c4f8d4f26744/IJBMS-23-439-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/64b0b7aa3273/IJBMS-23-439-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/ee449bdb46ba/IJBMS-23-439-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/f4251e92b5ed/IJBMS-23-439-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/87a00df4e2a7/IJBMS-23-439-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/53c0655242b3/IJBMS-23-439-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/5706be176f94/IJBMS-23-439-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/339caad7f376/IJBMS-23-439-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/6118cd590ebf/IJBMS-23-439-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/cca69d9896f9/IJBMS-23-439-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/c4f8d4f26744/IJBMS-23-439-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e31/7239430/64b0b7aa3273/IJBMS-23-439-g010.jpg

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