RESUMEN
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.