ABSTRACT
Objective:To analyze the effect of simvastatin combined with tanshinone in the treatment of patients with acute cere-bral infarction. Methods:The patients with acute cerebral infarction were randomly divided into the treatment group (n=50) and the control group (n=50). The control group was given tanshinone treatment, the treatment group was given simvastatin treatment addi-tionally, and the treatment course was 14 d. The NIHSS ( nerve function defect degree) , ADL ( daily life activity) and the treatment effect before and after the treatment were comprehensively evaluated and compared between the two groups. Results: Compared with those before the treatment, the NIHSS and ADL scores were significantly improved in the two groups after the treatment, and the differ-ences were statistically significant (P<0. 05), and the improvement in the treatment group was significantly better than that in the control group with statistical significance (P<0. 05). The total effective rate of the observation group was 98%, which was higher than that (70%) in the control group (P<0. 05). Conclusion: Simvastatin combined with tanshinone in the treatment of acute cerebral infarction shows obvious therapeutic effect, which can obviously improve neurologic deficits and daily life activity, and is worthy of fur-ther clinical application.
ABSTRACT
Objective Study the expressions of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) in rat models of cerebral ischemia reperfusion and the protective effect of ?-Sodium Aescinate.Methods Rat models of cerebral ischemia-reperfusion were made using an intraluminal monofilament method and ?-Sodium Aescinate was given peritoneally to observe its protective effect. The histochemical change and the expression of ICAM-1, VCAM-1 were detected by HE staining and immunohistochemistry ways.Results (1) ?-Sodium Aescinate could obviously reduce the brain damage after ischemia reperfusion. (2) The expressions of ICAM-1, VCAM-1 in endothelial cells in ischemic territory increased after cerebral ischemia reperfusion. ICAM-1 immunoreactivity peaked at 24 h after reperfusion and VCAM-1 immunoreactivity peaked at 24～48 h after reperfusion. Both of them decreased gradually, but remained a higher level than normal 72 h after reperfusion. (3) ?-Sodium Aescinate could decrease the expressions of ICAM-1, VCAM-1 remarkably 24 h and 48 h after reperfusion.Conclusions High expressions of ICAM-1, VCAM-1 may be involved in the mechanism of cerebral ischemia reperfusion injury. ?-Sodium Aescinate may play its protective role by reducing the expressions of ICAM-1 and VCAM-1.