**3. Conclusion**

Apoptotic response of hepatocytes through the binding of HMGB1 protein to *Gsto1* promoter region is caused in this experimental hepatitis model and GL‐treatment prevents the apopto‐ sis and inflammatory infiltrates caused with LPS/GalN‐injection by disturbing the binding of HMGB1 protein to *Gsto1* promoter sequence. The present findings claim a new mechanism supporting therapeutic effects of GL in hepatitis (**Figure 4**).

**Figure 4.** Action point of acetylated HMGB1. An administration of GL suppresses apoptotic cell death through inhibiting the binding of Hmgb1 to *Gsto1* (Scheme modified from Nature Reviews Immunology 2005:5:334).
