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评估颅内压升高和应激在 TBI 后海马细胞凋亡和下丘脑-垂体功能障碍中的作用。

Assessment of the role of intracranial hypertension and stress on hippocampal cell apoptosis and hypothalamic-pituitary dysfunction after TBI.

机构信息

Graduate School of Tianjin Medical University, Tianjin, 300070, China.

Department of Neurosurgery, Tianjin Huanhu Hospital, Tianjin, 300350, China.

出版信息

Sci Rep. 2017 Jun 19;7(1):3805. doi: 10.1038/s41598-017-04008-w.

DOI:10.1038/s41598-017-04008-w
PMID:28630478
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5476648/
Abstract

In recent years, hypopituitarism caused by traumatic brain injury (TBI) has been explored in many clinical studies; however, few studies have focused on intracranial hypertension and stress caused by TBI. In this study, an intracranial hypertension model, with epidural hematoma as the cause, was used to explore the physiopathological and neuroendocrine changes in the hypothalamic-pituitary axis and hippocampus. The results demonstrated that intracranial hypertension increased the apoptosis rate, caspase-3 levels and proliferating cell nuclear antigen (PCNA) in the hippocampus, hypothalamus, pituitary gland and showed a consistent rate of apoptosis within each group. The apoptosis rates of hippocampus, hypothalamus and pituitary gland were further increased when intracranial pressure (ICP) at 24 hour (h) were still increased. The change rates of apoptosis in hypothalamus and pituitary gland were significantly higher than hippocampus. Moreover, the stress caused by surgery may be a crucial factor in apoptosis. To confirm stress leads to apoptosis in the hypothalamus and pituitary gland, we used rabbits to establish a standard stress model. The results confirmed that stress leads to apoptosis of neuroendocrine cells in the hypothalamus and pituitary gland, moreover, the higher the stress intensity, the higher the apoptosis rate in the hypothalamus and pituitary gland.

摘要

近年来,外伤性脑损伤(TBI)引起的垂体功能减退症在许多临床研究中得到了探讨;然而,很少有研究关注 TBI 引起的颅内压升高和应激。在这项研究中,我们使用硬膜外血肿作为病因建立了颅内高压模型,以探讨创伤性脑损伤后下丘脑-垂体轴和海马体的病理生理和神经内分泌变化。结果表明,颅内压升高增加了海马体、下丘脑、垂体中的细胞凋亡率、caspase-3 水平和增殖细胞核抗原(PCNA),且每个组的细胞凋亡率均呈一致趋势。当 24 小时颅内压(ICP)仍升高时,海马体、下丘脑和垂体的细胞凋亡率进一步增加。下丘脑和垂体的细胞凋亡率变化率明显高于海马体。此外,手术引起的应激可能是细胞凋亡的关键因素。为了证实应激会导致下丘脑和垂体发生细胞凋亡,我们使用兔子建立了标准的应激模型。结果证实,应激导致下丘脑和垂体神经内分泌细胞凋亡,而且应激强度越高,下丘脑和垂体的细胞凋亡率越高。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/c2eb5cda8063/41598_2017_4008_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/85e3536c2e3f/41598_2017_4008_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/c9fd6dc052a5/41598_2017_4008_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/7a6b30bf1e55/41598_2017_4008_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/dbdfc216c838/41598_2017_4008_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/b76cef547111/41598_2017_4008_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/af26deef6b4b/41598_2017_4008_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/38d2bfe6d91d/41598_2017_4008_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/903494eca109/41598_2017_4008_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/c2eb5cda8063/41598_2017_4008_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/85e3536c2e3f/41598_2017_4008_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/c9fd6dc052a5/41598_2017_4008_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/7a6b30bf1e55/41598_2017_4008_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/dbdfc216c838/41598_2017_4008_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/b76cef547111/41598_2017_4008_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/af26deef6b4b/41598_2017_4008_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/38d2bfe6d91d/41598_2017_4008_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/903494eca109/41598_2017_4008_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c34a/5476648/c2eb5cda8063/41598_2017_4008_Fig9_HTML.jpg

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