Effects of beta-Aescin on the expression of nuclear factor-kappaB and tumor necrosis factor-alpha after traumatic brain injury in rats.

Abstract

To investigate the inhibiting effect of beta-Aescin on nuclear factor-kappaB (NF-kappaB) activation and the expression of tumor necrosis factor-alpha (TNF-alpha) protein after traumatic brain injury (TBI) in the rat brain, 62 SD rats were subjected to lateral cortical impact injury caused by a free-falling object and divided randomly into four groups: (1) sham operated (Group A); (2) injured (Group B); (3) beta-Aescin treatment (Group C); (4) pyrrolidine dithocarbamate (PDTC) treatment (Group D). Beta-Aescin was administered in Group C and PDTC treated in Group D immediately after injury. A series of brain samples were obtained directly 6 h, 24 h and 3 d respectively after trauma in four groups. NF-kappaB activation was examined by Electrophoretic Mobility Shift Assay (EMSA); the levels of TNF-alpha protein were measured by radio-immunoassay (RIA); the water content of rat brain was measured and pathomorphological observation was carried out. NF-kappaB activation, the levels of TNF-alpha protein and the water content of rat brain were significantly increased (P<0.01) following TBI in rats. Compared with Group B, NF-kappaB activation (P<0.01), the levels of TNF-alpha protein (P<0.01) and the water content of brain (P<0.05) began to decrease obviously after injury in Groups C and D. Beta-Aescin could dramatically inhibit NF-kappaB activation and the expression of TNF-alpha protein in the rat brain, alleviate rat brain edema, and that could partially be the molecular mechanism by which beta-Aescin attenuates traumatic brain edema.