چکیده (انگلیسی):

Objective: To explore the protection and molecular mechanism of histone deacetylase
inhibitors (HDACIs) on the spleen of rats with hemorrhagic shock.
Methods: A total of 60 SPF male SD rats were selected for the modeling of severe
hemorrhagic shock using the method of arterial and venous cannulation with the timedivided
bleeding. The measurement of mean arterial blood pressure and blood lactic
acid was used to verify the modeling. The modeled rats were randomly divided into shock
group, shock + suberoylanilide hydroxamic acid (SAHA) group, shock + autogenous
transfusion group and shock + SAHA + autogenous transfusion group. Three hours after
the treatment, the spleen of rats was collected and TUNEL method was employed to
detect the apoptosis of spleen cells in each group. The statistical analysis was performed.
Afterwards, real-time PCR and western blot were employed to detect the expression of
BCL-2, BAX and caspass3 in the spleen of rats in each group.
Results: A total of 53 rats had successful modeling of severe hemorrhagic shock, with
success rate of 88%. Cell apoptosis in the severe hemorrhagic model group was the most
serious. After the intervention of HDACIs and the autogenous transfusion, the tissue
injury was a bit recovered. Cell apoptosis was least in the shock + SAHA + autogenous
transfusion group (P < 0.05). After the intervention of HDACIs and the autogenous
transfusion, the relative expression of BCL-2 was significantly increased (P < 0.05), with
highest relative expression of BCL-2 in shock + SAHA + autogenous transfusion group
(P < 0.05). After the intervention of HDACIs and the autogenous transfusion, the relative
expression of BAX was significantly decreased (P < 0.05), with lowest relative
expression of BAX in the intervention group of single HDACIs. The change in the
expression of caspass3 was similar to BAX, namely the relative expression of caspass3
was significantly decreased after the intervention of HDACIs and the autogenous transfusion
(P < 0.05).
Conclusions: HDACIs and autogenous transfusion can all protect the spleen injury
because of the severe hemorrhagic shock. Its molecular mechanism may be related to the
regulation on the expression of BCL-2/BAX and caspass3, which may affect the
apoptosis process of cells.