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Abstract: To investigate the inhibiting effect of beta%29&ck%5b%5D=abstract&ck%5b%5D=keyword'>b>&beta;b%5D=abstract&ck%5b%5D=keyword'>b>-Aescin on b%5D=abstract&ck%5b%5D=keyword'>b>nuclear factor-&kappa;b (NF-κb) activation and the expression of tumor necrosis factor-&alpha; (TNF-α) 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%29&ck%5b%5D=abstract&ck%5b%5D=keyword'>b>&beta;b%5D=abstract&ck%5b%5D=keyword'>b>-Aescin treatment (Group C); (4) pyrrolidine dithocarbamate (PDTC) treatment (Group D). beta%29&ck%5b%5D=abstract&ck%5b%5D=keyword'>b>&beta;b%5D=abstract&ck%5b%5D=keyword'>b>-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-κb activation was examined by Electrophoretic Mobility Shift Assay (EMSA); the levels of TNF-α protein were measured by radio-immunoassay (RIA); the water content of rat brain was measured and pathomorphological observation was carried out. NF-κb activation, the levels of TNF-α protein and the water content of rat brain were significantly increased (P<0.01) following TbI in rats. Compared with Group b, NF-κb activation (P<0.01), the levels of TNF-α 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%29&ck%5b%5D=abstract&ck%5b%5D=keyword'>b>&beta;b%5D=abstract&ck%5b%5D=keyword'>b>-Aescin could dramatically inhibit NF-κb activation and the expression of TNF-α protein in the rat brain, alleviate rat brain edema, and that could partially be the molecular mechanism by which beta%29&ck%5b%5D=abstract&ck%5b%5D=keyword'>b>&beta;b%5D=abstract&ck%5b%5D=keyword'>b>-Aescin attenuates traumatic brain edema.

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