Dual function of methylprednisolone on paraventricular nucleus neurons after traumatic brain injury in rats
10.3760/cma.j.issn.1001-8050.2014.08.020
- VernacularTitle:甲基强的松龙对脑创伤后大鼠下丘脑室旁核神经元的双重作用
- Author:
Bin ZHANG
;
Julei WANG
;
Zhiguo ZHANG
;
Huaizhou QIN
- Publication Type:Journal Article
- Keywords:
Brain injuries;
Apoptosis;
Methylprednisolone;
Stress disorders,post-traumatic;
Paraventricular hypothalamic nucleus
- From:
Chinese Journal of Trauma
2014;30(8):831-837
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of methylprednisolone (MP) therapy on apoptosis of neurons in the paraventricular nucleus (PVN) after traumatic brain injury (TBI) in rats.Methods A total of 185 Wistar rats were divided into sham operation group (n =20),trauma control group (n =45),low-dose MP therapy group (n =50) and high-dose MP therapy group (n =70),according to the random number table.TBI models were induced by fluid percussion injury.TUNEL staining,immunohistochemistry and transmission electron microscope were used to detect PVN neuron number and apoptosis.Results Apoptotic neurons in the PVN were 0.7 ± 1.6,rare in sham operation group,whereas apoptotic neurons in trauma control group were firstly detected at 3 days and reached peak at 7 days (36.4 ± 18.8),with a slump of corticotropin-releasing hormone (CRH) for 208.0 ± 19.8.High-dose MP therapy markedly increased the neuron apoptosis (70.7±27.2),reduced CRH-positive cells (141.7 ±32.6),and increased short-term mortality (55％) when compared to trauma control group (all P ＜ 0.05).In contrast,low-dose MP greatly reduced PVN neuron apoptosis (17.6 ± 6.9),but increased CRH-positive cells (249.2 ±20.3) (P＜0.05) and decreased the short-term mortality (10％).Conclusions High-dose MP therapy increases neuronal apoptosis in PVN and short-term mortality after TBI.However,low-dose MP protects PVN neurons against TBI-induced apoptosis and reduces the mortality.
