OBJECTIVE: To observe the effect of chronic psychological stress on vascular endothelial dysfunction rats and to explore the intervention and mechanism of Tongxinluo (TXL) on it. METHODS: Forty male Wistar rats were randomly divided into the normal control group (with no modeling), the endothelial dysfunction group (the HCY group), the psychological stress group (the model group), and TXL group, ten in each group. Rats in the latter three groups were fed with 3% high methionine diet to duplicate vascular endothelial dysfunction (VED) model. In addition, chronic psychological stress was applied in VED rats using repeated binding method. TXL at the dose of 1.2 g/kg body weight was given by gastrogavage. The plasma endothelin (ET) and angiotensin II (Ang II), serum cortisone (CORT) were detected by radioimmunoassay. The serum nitric oxide (NO) was detected by nitrate reductase. Ultrastructural changes of aortic endothelial cells were observed by transmission electron microscope. Serum levels of norepinephrine (NE) and epinephrine (E) were detected by enzyme linked immunosorbent assay (ELISA). RESULTS: Compared with the plasma ET level and the serum NO level in the HCY group (161.70 +/- 13.96 pg/mL and 26.82 +/- 13.03 micromol/L), the plasma ET level obviously increased (178.25 +/- 21.85 pg/mL) (P < 0.05) and the serum NO level decreased (24.91 +/- 9.95 micromol/L, P > 0.05), levels of CORT, NE, and E obviously increased in the model group (all P < 0.05). Ultrastructural changes of aortic endothelial cells were obviously injured. Compared with the model group, the plasma ET level (154.74 +/- 13.27 pg/mL), Ang II, CORT, NE, and E obviously decreased (P < 0.05, P < 0.01), the serum NO level obviously increased (34.44 +/- 18.35 micromol/L, P < 0.05). Ultrastructural changes of aortic endothelial cells were obviously improved. CONCLUSIONS: Chronic psychological stress could obviously aggravate endothelial injury in VED rats. TXL showed protection on the vascular endothelial structure and function.
OBJECTIVE: To observe the effect of chronic psychological stress on vascular endothelial dysfunction rats and to explore the intervention and mechanism of Tongxinluo (TXL) on it. METHODS: Forty male Wistar rats were randomly divided into the normal control group (with no modeling), the endothelial dysfunction group (the HCY group), the psychological stress group (the model group), and TXL group, ten in each group. Rats in the latter three groups were fed with 3% high methionine diet to duplicate vascular endothelial dysfunction (VED) model. In addition, chronic psychological stress was applied in VED rats using repeated binding method. TXL at the dose of 1.2 g/kg body weight was given by gastrogavage. The plasma endothelin (ET) and angiotensin II (Ang II), serum cortisone (CORT) were detected by radioimmunoassay. The serum nitric oxide (NO) was detected by nitrate reductase. Ultrastructural changes of aortic endothelial cells were observed by transmission electron microscope. Serum levels of norepinephrine (NE) and epinephrine (E) were detected by enzyme linked immunosorbent assay (ELISA). RESULTS: Compared with the plasma ET level and the serum NO level in the HCY group (161.70 +/- 13.96 pg/mL and 26.82 +/- 13.03 micromol/L), the plasma ET level obviously increased (178.25 +/- 21.85 pg/mL) (P < 0.05) and the serum NO level decreased (24.91 +/- 9.95 micromol/L, P > 0.05), levels of CORT, NE, and E obviously increased in the model group (all P < 0.05). Ultrastructural changes of aortic endothelial cells were obviously injured. Compared with the model group, the plasma ET level (154.74 +/- 13.27 pg/mL), Ang II, CORT, NE, and E obviously decreased (P < 0.05, P < 0.01), the serum NO level obviously increased (34.44 +/- 18.35 micromol/L, P < 0.05). Ultrastructural changes of aortic endothelial cells were obviously improved. CONCLUSIONS: Chronic psychological stress could obviously aggravate endothelial injury in VED rats. TXL showed protection on the vascular endothelial structure and function.