The incidence of critical-illness-related-corticosteroid-insufficiency is associated with severity of traumatic brain injury in adult rats

2014 ◽  
Vol 342 (1-2) ◽  
pp. 93-100 ◽  
Author(s):  
Xin Chen ◽  
Zilong Zhao ◽  
Yan Chai ◽  
Lanlan Luo ◽  
Rongcai Jiang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Critical Illness ◽  
Adult Rats ◽  
Corticosteroid Insufficiency

scholarly journals Corticosteroid receptor rebalancing alleviates critical illness-related corticosteroid insufficiency after traumatic brain injury by promoting paraventricular nuclear cell survival via Akt/CREB/BDNF signaling

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Bin Zhang ◽  
Miao Bai ◽  
Xiaojian Xu ◽  
Mengshi Yang ◽  
Fei Niu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Critical Illness ◽  
Low Dose ◽  
Cell Loss ◽  
High Dose ◽  
Protective Effects ◽  
Signaling Mechanism ◽  
High Dose Methylprednisolone ◽  
Corticosteroid Insufficiency

Abstract Background We previously found that high-dose methylprednisolone increased the incidence of critical illness-related corticosteroid insufficiency (CIRCI) and mortality in rats with traumatic brain injury (TBI), whereas low-dose hydrocortisone but not methylprednisolone exerted protective effects. However, the receptor-mediated mechanism remains unclear. This study investigated the receptor-mediated mechanism of the opposite effects of different glucocorticoids on the survival of paraventricular nucleus (PVN) cells and the incidence of CIRCI after TBI. Methods Based on controlled cortical impact (CCI) and treatments, male SD rats (n = 300) were randomly divided into the sham, CCI, CCI + GCs (methylprednisolone 1 or 30 mg/kg/day; corticosterone 1 mg/kg/day), CCI + methylprednisolone+RU486 (RU486 50 mg/kg/day), and CCI + corticosterone+spironolactone (spironolactone 50 mg/kg/day) groups. Blood samples were collected 7 days before and after CCI. Brain tissues were collected on postinjury day 7 and processed for histology and western blot analysis. Results We examined the incidence of CIRCI, mortality, apoptosis in the PVN, the receptor-mediated mechanism, and downstream signaling pathways on postinjury day 7. We found that methylprednisolone and corticosterone exerted opposite effects on the survival of PVN cells and the incidence of CIRCI by activating different receptors. High-dose methylprednisolone increased the nuclear glucocorticoid receptor (GR) level and subsequently increased cell loss in the PVN and the incidence of CIRCI. In contrast, low-dose corticosterone but not methylprednisolone played a protective role by upregulating mineralocorticoid receptor (MR) activation. The possible downstream receptor signaling mechanism involved the differential effects of GR and MR on the activity of the Akt/CREB/BDNF pathway. Conclusion The excessive activation of GR by high-dose methylprednisolone exacerbated apoptosis in the PVN and increased CIRCI. In contrast, refilling of MR by corticosterone protects PVN neurons and reduces the incidence of CIRCI by promoting GR/MR rebalancing after TBI.

A comparison of different models with motor dysfunction after traumatic brain injury in adult rats

2014 ◽  
Vol 13 (04) ◽  
pp. 579-593 ◽  
Author(s):  
Meng Wang ◽  
Hongjian Pu ◽  
Yingchao Liu ◽  
Zengtao Wang ◽  
Bomin Wang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Motor Dysfunction ◽  
Adult Rats

Cell Proliferation in the Brains of Adult Rats Exposed to Traumatic Brain Injury

2013 ◽  
pp. 27-38
Author(s):  
Sandra A. Acosta ◽  
Naoki Tajiri ◽  
Paula C. Bickford ◽  
Cesar V. Borlongan
Keyword(s):  
Traumatic Brain Injury ◽  
Cell Proliferation ◽  
Brain Injury ◽  
Adult Rats

Spatial and temporal dynamics of HDACs class IIa following mild traumatic brain injury in adult rats

2022 ◽  
Author(s):  
Swatabdi R. Kamal ◽  
Shreya Potukutchi ◽  
David J. Gelovani ◽  
Robin E. Bonomi ◽  
Srinivasu Kallakuri ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Temporal Dynamics ◽  
Adult Rats ◽  
Spatial And Temporal Dynamics

Intracranial bone marrow transplantation after traumatic brain injury improving functional outcome in adult rats

2001 ◽  
Vol 94 (4) ◽  
pp. 589-595 ◽  
Author(s):  
Asim Mahmood ◽  
Dunyue Lu ◽  
Yi Li ◽  
Jae Li Chen ◽  
Michael Chopp
Keyword(s):  
Traumatic Brain Injury ◽  
Bone Marrow ◽  
Brain Injury ◽  
Motor Function ◽  
Glial Fibrillary Acid Protein ◽  
Protein Markers ◽  
Adult Rats ◽  
Content Type ◽  
The Impact ◽  
Fine Print

Object. The authors tested the hypothesis that intracranial bone marrow (BM) transplantation after traumatic brain injury (TBI) in rats provides therapeutic benefit. Methods. Sixty-six adult Wistar rats, weighing 275 to 350 g each, were used for the experiment. Bone marrow prelabeled with bromodeoxyuridine (BrdU) was harvested from tibias and femurs of healthy adult rats. Other animals were subjected to controlled cortical impact, and BM was injected adjacent to the contusion 24 hours after the impact. The animals were killed at 4, 7, 14, or 28 days after transplantation. Motor function was evaluated both before and after the injury by using the rotarod test. After the animals had been killed, brain sections were examined using hemotoxylin and eosin and immunohistochemical staining methods. Histological examination revealed that, after transplantation, BM cells survived, proliferated, and migrated toward the injury site. Some of the BrdU-labeled BM cells were reactive, with astrocytic (glial fibrillary acid protein) and neuronal (NeuN and microtubule-associated protein) markers. Transplanted BM expressed proteins phenotypical of intrinsic brain cells, that is, neurons and astrocytes. A statistically significant improvement in motor function in rats that underwent BM transplantation, compared with control rats, was detected at 14 and 28 days posttransplantation. Conclusions. On the basis of their findings, the authors assert that BM transplantation improves neurological outcome and that BM cells survive and express nerve cell proteins after TBI.

CORTICOSTEROID INSUFFICIENCY AFTER TRAUMATIC BRAIN INJURY.

2004 ◽  
Vol 52 ◽  
pp. S383
Author(s):  
P. Cohan ◽  
B. Armin ◽  
P. D. Christenson ◽  
D. McArthur ◽  
N. Mirza ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Corticosteroid Insufficiency
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