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

Figure 4

Inhibition of HMGB1 decreased brain edema, prevented the disruption of BBB, alleviated axonal injury, and improved the neurological deficits. Pretreatment with GL significantly improved the neurological outcomes compared with saline pretreatment after DAI (a). Brain edema evaluation showed that BWC in DAI + GL group was significantly reduced compared with DAI + NS group (b). The general observation of Evans blue in rat brains after DAI in different groups (c). The quantitative analysis showed that the Evans blue level in DAI + GL group was much lower compared with DAI + NS group, although still above the control level (d). Protective effect of GL on the axonal injury after DAI as demonstrated by the immunohistochemical staining of β-APP. Pretreatment with GL dramatically reduced the accumulation of β-APP compared with saline pretreatment group, which indicated a reduced structural axonal injury after DAI (e). compared with control group; compared with DAI + saline group.

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