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XH induction of apoptosis at high concentrations. XH treatment initiates intrinsic and extrinsic apoptosis pathways by multiple mechanisms, including downregulation of antiapoptotic (BCL-2) and induction of pro-apoptotic (Bax) proteins, increases in ROS, leading to decreased mitochondrial membrane potential and subsequent cytochrome C release, and activation of caspases. As a result, cleavage of PARP and reduced proliferation of tumor cells has been observed after XH treatments.72–75
