ABSTRACT
The prevention of myocardial and brain dysfunction induced by positive acceleration (+Gz) exposure is the focus in the field of aerospace medicine research topic .The characteristics and mechanisms that +Gz exposure caused damages to vital organs such as heart and brain remain to be further elucidated .The research literature about +Gz acceleration exposure-induced heart and brain injuries in experimental animals and its mechanisms at home and abroad was reviewed in this paper .
ABSTRACT
Objective To study the effect of rhodiola crenulata compound on serum corticosterone and myocardial glucocorticoid receptor ( GR) in rats exposed high sustained +Gz.Methods Seventy-two healthy SD rats were randomly divided into six groups: blank control group, stress control group, +10 Gz stress group and low, medium, high dose drug group, with twelve rats in each.20 mL/kg menstruum was fed to each rat once per day for 14 days.Low, medium and high dose drug group were fed with rhodiola crenulata compound at doses of 0.75 g/kg, 1.5 g/kg and 3.0 g/kg respectively, the other three groups were fed with equal volume saline.Rats were exposed to high +Gz in 15th day.The concentration of corticosterone in the serum of each group rats was detected with ELISA. Western blot was used to detect the expressions of GR in the myocardium of each group rats .Results The content of corticosterone was significantly elevated in +10Gz stress group, while the expression of GR in the myocardium was markedly declined (P <0.01,P <0.05).However, compound preconditioning could decrease concentration of corticosterone in the serum and enhance the expression of GR in the myocardium from rats after +10 Gz exposure. The corticosterone concentration of medium and high dose drug groups was significantly lower and the level of GR expression in the myocardium was significantly higher than that of +10 Gz stress group ( P <0.05 , P <0.01 ) . Conclusion Rhodiola crenulata compound preconditioning could regulate the concentration of corticosterone in the serum and the level of GR expression in the myocardium of the rats exposed +10 Gz, which may be related with its protective effect on high sustained +Gz-induced injury of myocardium.
ABSTRACT
Objectives: To observe the roles of nuclear factor ?B(NF ?B) in corticosterone injured hippocampal neurons. Methods:Two groups of primary hippocampal neurons were cultured for 8～10 days. One group was treated with 1?10 -5 mol/L corticosterone. The total cellular nuclear protein levels were extracted at 0.5,1,2 and 4 hours, respectively. Electrophoresis mobility shift assay (EMSA) was used to detect the expression of NF ?B activation. Another group was treated with ?B decoy DNA(25 ?mol/L) to inhibit the activity of NF ?B for 2 hours before 1?10 -5 mol/L corticosterone was intervened. MTT was used to observe the effects of corticosterone induced neurons injury after 6,12,24 and 48 hours. Results:The activity of NF ?B became significantly lower than that in the control group after corticosterone acted on neurons for 1 hour. As time went on, its effects became more conspicuously. The injury of hippocampal neurons aggravated when the activity of NF ?B was inhibited by ?B decoy DNA. Conclusions: NF ?B plays a protective role in corticosterone induced hippocampal neuron injury.