Oxidative Medicine and Cellular Longevity / 2017 / Article / Fig 7

Research Article

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.

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