The peeling process of fresh ginger during factory production causes not only waste but also pollution to the environment. Now, by fermenting whole pieces of fresh ginger into black ginger, people are able to further enhance the nutritional value of ginger while lowering the burden on the environment. In this experiment, fresh ginger was fermented into black ginger, and superoxide dismutase (SOD) crudely extracted from both fresh ginger and black ginger were gavaged separately in type 2 diabetic rats to compare the SOD activity and effect in rat liver during the treatment of type 2 diabetes. It was found that the SOD activity of extracts from fermented black ginger was much higher than that of extracts from fresh ginger. In addition, the activity of SOD in the liver of rats gavaged with black ginger extract is higher than that in the liver of rats gavaged with fresh ginger extract, which shows that black ginger extract has certain protective effects on the liver.

Apoptosis plays a crucial role for generation of lymphocyte repertoire, clonal contraction, and elimination of virus-infected cells. Since IL-3-dependent pro-B cell line Baf-3 resulted in rapid induction of apoptotic cell death upon IL-3 withdrawal, it would by very valuable for analysis of apoptosis induction by growth factor deprivation. First, we confirmed that Baf-3 cells underwent loss of mitochondrial membrane potential (ΔΨm) and apoptosis in a time-dependent manner when they were cultured in the RPMI-1640 medium without IL-3. Induction of apoptosis and loss of ΔΨm was determined by DiOC6 and annexin V staining method using flow cytometer, respectively. Deprivation of IL-3 induced upregulation of proapoptotic molecule Bax, in conjunction with slight down-regulation of anti-apoptotic molecule Bcl-xL, which was assessed by Western blotting. Since Bcl-xL-overexpressing Baf-3 cells showed some resistance to IL-3-deprivation, Bcl-xL prevents apoptosis induced by IL-3 withdrawal. Finally, a sustained JNK1 activation was observed prior to induction of apoptosis upon IL-3 deprivation. Dominat-negative form of JNK1 and JNK inhibitor sp600125 partially inhibit the apoptosis upon IL-3 deprivation, suggesting that a sustained JNK1 activation was involved in the induction of apoptosis. Together, IL-3 deprivation of IL-3-dependent cell line Baf-3 induces a sustained JNK1 activation, followed by a decline of the ratio of Bcl-xL to Bax, leading to loss of DCm, and finally apoptosis.