Inhibiting HMGB1 with Glycyrrhizic Acid Protects Brain Injury after DAI via Its Anti-Inflammatory Effect

Figure 3

GL pretreatment reduced neuronal apoptosis by inhibiting the expression and cytosolic release of HMGB1 at 24 h after DAI. GL was administrated 30 min before the induction of DAI at a dose of 10 mg/kg, significantly reducing neuronal apoptosis compared with DAI + NS group (a). Western blot showed that the cleavage of caspases 3 and 9 and the phosphorylation of BCL-2 were suppressed by GL pretreatment compared with DAI + NS group (b). Immunofluorescence showed that HMGB1 was mainly present in the nucleus of neuronal cells, and no clear expression was found in the cytosol of the control rat brains. At 24 h after DAI, the cytosolic HMGB1 increased, and the nuclear HMGB1 showed a simultaneous slight decrease (data not shown). After GL pretreatment, the cytosolic expression of HMGB1 was clearly suppressed (c). compared with control group; compared with DAI + saline group.

(a)

(b)

(c)