RESUMO
Objective To investigate the expression of hypoxia-inducible factor-1α (HIF-1α) in patients with traumatic brain injury (TBI) and their clinical significance. Methods Peripheral blood and brain tissue samples were obtained from 60 TBI patients. According to the GCS score, 60 TBI patients were divided into the moderate damage group, the severe damage group and the especially severe damage group. According to the different time points after the injury, the patients were divided into <6 hours group, 6-24 hours group, 24-72 hours group and >72 hours group. The 60 control brain tissue samples were obtained from patients with cerebral aneurysms and undergoing craniotomy at the same time; and control peripheral blood were collected from 60 healthy people. The levels of HIF-1α were measured with RT-PCR and Western blot . One-way ANOVA and t-test were used to analyze the results with SPSS 18.0. Results The expression of HIF-1α in the control group [peripheral blood: HIF-1α mRNA (0.35±0.12), HIF-1α protein (0.28±0.06) ;brain tissue: HIF-1α mRNA (0.65±0.08),HIF-1α protein (0.78±0.08)] was obviously lower than those in the TBI groups, and the differences were statistically significant (P<0.05). Along with the damage degree aggravating, the expression of HIF-1α was increased. The expression of HIF-1α in the especially severe damage group was statistically higher than those of the severe damage group and the moderate damage group (P<0.05). The expression of HIF-1α was increased along with the extension of time after the injury. The expression of HIF-1α in the 24-72 h group was significantly higher than those of the >72 h group, 6-24 h group and <6 h group (P<0.05). Conclusions The expression of HIF-1α is closely related to the severity of TBI and may play an important role in the progress of TBI.
RESUMO
Objective To investigate the effect of breviscapine on the proliferation and the expression of thrombin receptor mRNA of vascular smooth muscle cells (VSMCs) . Methods Rat thoracic aortic VSMCs cultivated in vitro were randomly assigned to control,breviscapine 0.5 μg/mL, 5 μg/mL and 50 μg/mL groups, The proliferation was induced by thrombin, The proliferative effect of VSMCs was measured by the3H-thymidine (3H-TdR) incorporation method; the expression intensity of thrombin receptor mRNA relative to β-actin mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR). Results The incorporation rate (cpm/1. 5 × 105 cells) of3H-TdR were 1 216. 00±241.57,673.25±12.63,602.50±80.59, and 522.00±103.99 respectively in the control, and breviscapine 0. 5 μg/mL, 5 μg/mL and 50 μg/mL groups. As compared with the control group, the prolifera-tion of rat thoracic aortic VSMCs was inhibited significantly in all breviscapine groups (all P<0.05). RT-PCR showed that the expressions of thrombin receptor mRNA relative to β-actin mRNA were 0. 614, 0. 389, 0. 310, and 0. 280 respectively in the control, and breviscapine 0. 5μg/mL, 5μg/mL and 50 μg/mL groups, The expression ratios of TR/β-actin mRNA in thoracic aortic VSMCs in all the breviscapine groups were lower than those in the control group, which suggesting that the expression of thrombin receptor mRNA was inhibited. Conclusions Breviscapine inhibits the proliferation of rat VSMCs. Its mechanism may he associated with the inhibition of the thrombin receptor gene expression of VSMCs.