Progesterone treatment normalizes the levels of cell proliferation and cell death in the dentate gyrus of the hippocampus after traumatic brain injury.
Progesterone treatment normalizes the levels of cell proliferation and cell death in the dentate gyrus of the hippocampus after traumatic brain injury.
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孕酮治疗使外伤性脑损伤后海马齿状回的细胞增殖和细胞死亡水平归一化。
DOI：
10.1016/j.expneurol.2011.05.016
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发表时间：
2011-09
影响因子：
5.3
通讯作者：
Stein, Donald G.
中科院分区：
文献类型：
--
作者：
Barha, Cindy K.;Ishrat, Tauheed;Epp, Jonathan R.;Galea, Liisa A. M.;Stein, Donald G.
创伤性脑损伤(TBI)增加海马区细胞死亡，损害海马区依赖的认知。在人的一生中，海马体也是持续的神经发生的场所。脑损伤后给予黄体酮治疗可改善行为恢复，减少炎症、细胞凋亡、病变体积和水肿。本研究的目的是确定黄体酮是否改变了脑外伤后齿状回的细胞增殖和短期存活。双侧额叶皮质挫伤或假手术的雄性SD大鼠在术后1、6小时和每天至术后第7天接受黄体酮或赋形剂治疗，伤后48小时单次注射溴脱氧尿苷(BrdU)。然后对大脑进行Ki67(细胞增殖的内源性标记)、BrdU(短期细胞存活)、Doublectin(未成熟神经元的内源性标记)和Fluoro-Jade B(变性神经元的标记)的处理。与假手术相比，TBI可促进细胞增殖，黄体酮可使损伤大鼠的细胞增殖正常化。单独使用黄体酮可以促进正常大鼠的细胞增殖。有趣的是，损伤和/或黄体酮处理并不影响BrdU-ir细胞的短期细胞存活。所有治疗都增加了与Doublecortin(在这种情况下是标记存活5天的新神经元的未成熟神经元标记物)共同标记的BrdU-ir细胞的百分比，表明细胞命运独立于TBI和黄体酮治疗。脑损伤后存活5天的未成熟神经元数量增加，但黄体酮治疗降低了这一效应。此外，损伤增加了细胞死亡，黄体酮治疗减少了细胞死亡，达到了完整大鼠的水平。总之，这些发现表明，脑损伤后孕酮治疗使海马齿状回的细胞增殖和细胞死亡水平正常化。
Traumatic brain injury (TBI) increases cell death in the hippocampus and impairs hippocampus-dependent cognition. The hippocampus is also the site of ongoing neurogenesis throughout the lifespan. Progesterone treatment improves behavioral recovery and reduces inflammation, apoptosis, lesion volume, and edema, when given after TBI. The aim of the present study was to determine whether progesterone altered cell proliferation and short-term survival in the dentate gyrus after TBI. Male Sprague-Dawley rats with bilateral contusions of the frontal cortex or sham operations received progesterone or vehicle at 1 and 6 hours post-surgery and daily through post-surgery Day 7, and a single injection of bromodeoxyuridine (BrdU) 48 hours after injury. Brains were then processed for Ki67 (endogenous marker of cell proliferation), BrdU (short-term cell survival), doublecortin (endogenous marker of immature neurons), and Fluoro-Jade B (marker of degenerating neurons). TBI increased cell proliferation compared to shams and progesterone normalized cell proliferation in injured rats. Progesterone alone increased cell proliferation in intact rats. Interestingly, injury and/or progesterone treatment did not influence short-term cell survival of BrdU-ir cells. All treatments increased the percentage of BrdU-ir cells that were co-labeled with doublecortin (an immature neuronal marker in this case labelling new neurons that survived 5 days), indicating that cell fate is influenced independently by TBI and progesterone treatment. The number of immature neurons that survived 5 days was increased following TBI, but progesterone treatment reduced this effect. Furthermore, injury increased cell death and progesterone treatment reduced cell death to levels seen in intact rats. Together these findings suggest that progesterone treatment after TBI normalizes the levels of cell proliferation and cell death in the dentate gyrus of the hippocampus.
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影响因子：
4.1
作者：
Batarseh, Amani;Papadopoulos, Vassilios
通讯作者：
Papadopoulos, Vassilios
影响因子：
4.2
作者：
Djebaili, M;Guo, QM;Stein, DG
通讯作者：
Stein, DG
影响因子：
2.6
作者：
Ariza, Mar;Serra-Grabulosa, Josep M.;Sahuquillo, Juan
通讯作者：
Sahuquillo, Juan
影响因子：
3.2
作者：
Barha, C. K.;Lieblich, S. E.;Galea, L. A. M.
通讯作者：
Galea, L. A. M.
影响因子：
2.5
作者：
Brown, JP;Couillard-Després, S;Kuhn, HG
通讯作者：
Kuhn, HG