Beneficial effects of taurine on cardiac abnormality in NZB/W F1 mice fed with a high-cholesterol diet.

A significantly higher prevalence of cardiovascular disease (CVD) is reported in patients with systemic lupus erythematosus (SLE) as compared with the general population and accounts for approximately 30% of deaths in SLE patients. However, the mechanism of and treatments for CVD in patients with SLE are still unclear. To explore the effects of taurine on cardiac abnormality in SLE, NZB/W F1 mice were used as the experimental model by receiving control, cholesterol, or cholesterol/taurine diets, respectively. Improved cardiac histopathological changes were observed in left ventricle tissues from the cholesterol/taurine group as compared to the control or cholesterol group. Significant reductions of TUNEL-positive cells, Fas death receptor-related components, mitochondrial-dependent apoptosis, cardiac fibrosis, and fibrotic signaling components were detected in the left ventricle tissues from the cholesterol/taurine group as compared to the control or cholesterol group. Additionally, cardiac IGR1R survival signaling components were significantly increased in the left ventricle tissues from the cholesterol/taurine group as compared to the control or cholesterol group. These findings revealed the protective effects of taurine against the cardiac abnormalities in NZB/W F1 mice and may suggest the potential for clinical application of taurine in treatment of CVD in SLE.

Treatment with taurine attenuates hepatic apoptosis in NZB/W F1 mice fed with a high-cholesterol diet.

Cholesterol-rich diets are known to cause hepatic apoptosis, which has been associated with the pathogenesis of systemic lupus erythematosus (SLE). However, the mechanisms and treatments for hepatic apoptosis in SLE are poorly understood. To clarify the effects of taurine on hepatic apoptosis in SLE, NZB/W F1 mice received control, cholesterol, and cholesterol/taurine diets. Significant reductions of caspase-3 activity, TUNEL-positive cells, and Fas- and mitochondrial- dependent apoptosis were detected in liver from the cholesterol/taurine group as compared to the cholesterol group. Moreover, significant increases of phosphorylated AKT, NF-kappaB (p65), and ERK1/2 proteins were detected in liver from the cholesterol/taurine group as compared to the cholesterol group. In contrast, a significant reduction of phosphorylated p38 protein was observed in the cholesterol/taurine group. These experimental results demonstrated positive effects of taurine against hepatic apoptosis in NZB/W F1 mice fed a high-cholesterol diet and suggested the therapeutic potential of taurine in SLE.

Treatment with cystamine reduces apoptosis in liver from NZB/W F1 mice.

Increased population with hepatic diseases and apoptosis were found in patients with SLE and implicated in the pathogenesis of SLE. Since cystamine has been demonstrated to be beneficial to NZB/W F1 mice in our previous report, this study intends to investigate the effects of cystamine in liver from NZB/W F1 mice. Decreased apoptosis was detected in liver from NZB/W F1 mice given cystamine as compared to those given PBS by TUNEL and caspase-3 activity assay. Fas-dependent apoptotic proteins including Fas, cleaved caspase-8 and tBid were reduced in liver from NZB/W F1 mice given cystamine as compared to those given PBS. Additionally, the mitochondria-dependent apoptotic proteins including cytochrome c and Apaf-1 were reduced in liver from NZB/W F1 mice given cystamine as compared to those given PBS. Moreover, increased BCL-2 protein was observed in liver from both mice. Notably, increased NF-kappaB protein was detected in liver from NZB/W F1 mice given cystamine as compared to those given PBS. These experimental results suggest the effect of cystamine in reducing apoptosis in liver from NZB/W F1 mice through Fas-dependent and mitochondrial-dependent pathways. The phosphorylation of NF-kappaB (p65) could be a possible mechanism involving anti-apoptotic effects of cystamine in liver from NZB/W F1 mice.