Baicalin Ameliorates Experimental Liver Cholestasis in Mice by Modulation of Oxidative Stress, Inflammation, and NRF2 Transcription Factor

Figure 7

Baicalin markedly attenuated BDL-induced apoptotic and necrotic cell death markers DNA fragmentation, caspase 3 activity, and PARP activity in mouse liver. BDL induced significant increases in liver DNA fragmentation and caspase 3 activity, both markers of apoptotic cell death (a). BDL induced significant increase in PARP activity, a marker of necrotic and apoptotic cell death (b). BDL-induced increases in all three cell death markers were attenuated by baicalin treatment. Results are mean ± S.E.M. /group. versus control and ^# versus BDL.

(a)

(b)