Protective effects of black onion polysaccharide on liver and kidney injury in T2DM rats through the synergistic impact of hypolipidemic and antioxidant abilities.

In this study, the synergistic effects of black onion on the hypolipidemic and antioxidant activities in T2DM rats induced by a high-fat-diet and alloxan were investigated. The results showed that the fasting blood glucose of diabetic rats was significantly decreased after treatment with black onion polysaccharide (p < 0.01). Blood lipid analysis indicated that black onion polysaccharide could significantly improve the abnormal metabolism of blood lipids caused by diabetes. In addition, the MDA and ROS of the diabetic rats treated with black onion polysaccharide were significantly reduced; moreover, SOD was increased, indicating the excellent antioxidant activity of black onion polysaccharide. A histological examination clearly showed that black onion polysaccharide could improve the histological morphology of the liver and kidney. Furthermore, the indices of liver and kidney function were restored. These results indicate that black onion polysaccharide can reduce blood glucose and simultaneously show synergistic effects of hypoglycemic and antioxidant activities in diabetic rats. Therefore, black onion polysaccharide may alleviate liver and kidney function injury by improving the "two-hit" mechanism and can thus be used as a potential functional food to prevent diabetes and its complications.

Role of c-Jun N-terminal kinase activation in apoptosis induced by removal of the growth factors.

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.