RESUMEN
OBJECTIVE: To observe the effect of Panax notoginseng (PN) on pathological features in chronic subdural hematoma (CSDH) rabbits and its mechanisms. METHODS: A stable pathological animal model similar to CSDH in humans could be established using subdural injections of small number of blood through a subdural pre-catheter in rabbits. After successful modeling, 18 rabbits were randomly divided into the model group, the low dose PN group (0.125 g/kg), and the high dose PN group (0.250 g/kg), 6 in each group. Normal saline was given to rabbits in the model group, while PN power was given to those in the PN groups by gastrogavage for 6 successive days. Pathologic features of the hematoma outer membrane were observed by HE staining. The activity of SOD and the content of MDA in the hematoma outer membrane were examined by the colorimetric method. Expressions of CD31, CD34, and VEGF in the hematoma outer membrane were observed by immunohistochemical assay. Expressions of VEGF in the peripheral blood and the subdural hematoma were detected by enzyme-linked immunosorbent assay (ELISA). Expressions of VEGFR-1 and VEGFR-2 in the hematoma outer membrane were detected by Western blot. RESULTS: Compared with the model group, the inflammatory reaction was comparatively lessen and the proliferation of the fibrous tissue was relatively mature in the low and high dose PN groups. The activity of SOD increased (P < 0.05); expressions of CD31 and CD34 were reduced (P < 0.01); VEGF expression in the residual hematoma fluid decreased (P < 0.05) in the high dose PN group. Expressions of VEGF and VEGFR-2 were all reduced in the high and low dose PN groups (P < 0. 05, P < 0.01). Compared with the low dose PN group, expressions of CD31 and CD34 were reduced (P < 0.01), and the VEGFR-2 expression was also reduced (P < 0.05) in the high dose PN group. CONCLUSIONS: PN could promote the fibrous repairing of subdural hematoma in CSDH rabbits. It also lessened inflammation and oxidative injury of the hematoma outer membrane and reduced expressions of VEGF. The pathological angiogenesis could be reduced through influencing VEGFR-2 receptor pathways, which might be an important mechanism.