Objective To explore the significance of abnormal lipid metabolism induced by hypoxia in mice with pulmonary hypertension.Methods Thirty male C57BL/6 mice were chosen and were randomly divided into the model group and the control group, each consisting of 15 animals.The mice in the model group were exposed to chronic hypoxia for the development of hypoxic pul -monary hypertension model , and the mice in the control group were housed in the chamber at the normal ambient air .Right heart cathe-terization was used to measure right ventricular systolic pressure in the 2 groups, Masson method was used to observe the small pulmona-ry vascular vessel remodeling , and the ELISA method was used to detect levels of high density lipoprotein ( HDL-C) , cholesterol ( TC) and low density lipoprotein (LDL-C).The expressions of HMG-CoA reductase (HMGCR), low density lipoprotein receptor (LDLR) and ATP binding cassette transporter A1 (ABCA1) gene in the liver tissue were detected by real-time quantitative PCR.Results The right ventricular systolic pressure (40.12 ±8.22) mmHg(1 mmHg=0.133 kPa) and right ventricular hypertrophy index (0.352 ± 0.050) in the model group were significantly higher than those in the control group (P<0.05).The pulmonary artery vascular wall of the model group was significantly thicker than that of the control group .The HDL-C level of the model group was (26.20 ±3.73) mg/dl, which was significantly lower than that of the control group (P<0.05).There was no statistical significance in the levels of TC and

Objective To investigate the effects of vagus nerve electrostimulation (VNS) on the brain damage of rat middle cerebral artery occlusion (MCAO)/reperfusion model and its mechanism. Methods Twenty four adult male SD rats were randomly divided into two groups (12 each): MCAO/reperfusion group (MCAO group) and MCAO/reperfusion+VNS group (MCAO+VNS group). Subsequently, the neurological function deficit was determined by neurological scoring according to Zea Long scoring method 24h after MCAO/reperfusion. The cerebral infarction volume was determined by TTC assay. The cell apoptosis in brain damage zone was determined by TUNEL assay. Then, the effect of VNS on cAMP response element binding protein (CREB) and p-CREB protein expression was determined by Western blotting. The effect of VNS on Bcl-2 and Bax expression was determined by immunohistochemistry assay. Results Compared with MCAO group, VNS significantly inhibited MCAO-induced neurological deficit (P<0.01), decreased brain infarct volume (P<0.01) and cell apoptosis (P<0.01), increased the expression of p-CREB protein (P<0.01) and the number of Bcl-2-position cells (P<0.01) together with decreasing the number of Bax-position cells (P<0.01). However, VNS did not affect the expression of CREB protein (P>0.05). Conclusion VNS may ameliorate MCAO-induced neurological deficit and decrease brain infarct volume, which may be related to the promotion of p-CREB protein expression level.