Salvianolic acid B attenuates apoptosis and inflammation via SIRT1 activation in experimental stroke rats.

Silent information regulator 1 (SIRT1), a histone deacetylase, has been suggested to be effective in ischemic brain diseases. Salvianolic acid B (SalB) is a polyphenolic and one of the active components of Salvia miltiorrhiza Bunge. Previous studies suggested that SalB is protective against ischemic stroke. However, the role of SIRT1 in the protective effect of SalB against cerebral ischemia has not been explored. In this study, the rat brain was subjected to middle cerebral artery occlusion (MCAO). Before this surgery, rats were intraperitoneally administrated SalB with or without EX527, a specific SIRT1 inhibitor. The infarct volume, neurological score and brain water content were assessed. In addition, levels of TNF-α and IL-1ß in the brain tissues were detected by commercial ELISA kits. And the expression levels of SIRT, Ac-FOXO1, Bcl-2 and Bax were detected by Western blot. The results suggested that SalB exerted a cerebral-protective effect, as shown by reduced infarct volume, lowered brain edema and increased neurological scores. SalB also exerted anti-inflammatory effects as indicated by the decreased TNF-α and IL-1ß levels in the brain tissue. Moreover, SalB upregulated the expression of SIRT1 and Bcl-2 and downregulated the expression of Ac-FOXO1 and Bax. These effects of SalB were abolished by EX527 treatment. In summary, our results demonstrate that SalB treatment attenuates brain injury induced by ischemic stoke via reducing apoptosis and inflammation through the activation of SIRT1 signaling.

Nanobacteria: a possible etiology for type III prostatitis.

PURPOSE: Nanobacteria are thought to be a pathopoiesis bacterium in urological disease. We observed pathological changes in nanobacteria infected prostates in Sprague-Dawley(R) rats and investigated the possible etiological relationships of nanobacteria and type III prostatitis. MATERIALS AND METHODS: We randomized 40 adult male Sprague-Dawley rats each to the control and model groups. Rat prostate infection models were reproduced by infusing nanobacteria suspension transurethrally. Rats were sacrificed 1, 2, 4 and 8 weeks later, respectively. Prostatic pathology, and the cytokines interleukin-1beta and tumor necrosis factor-alpha were assessed. Nanobacteria isolation, culture and characterization were also analyzed. RESULTS: In model rats we observed prostatic acute inflammatory changes 1 to 2 weeks after nanobacteria infusion and chronic inflammatory changes after 4 weeks. At 8 weeks we noted microcalculous formation in the prostatic glandular cavity in 7 of the 10 model rats, which was not seen in controls. Interleukin-1beta and tumor necrosis factor-alpha in prostatic tissues were higher in model rats than in controls at different time points (p <0.01). In model rats interleukin-1beta and tumor necrosis factor-alpha were higher 2 weeks after infusion than at 1, 4 and 8 weeks (p <0.05). Prostatic tissue was nanobacteria positive in 35 model rats and in 0 controls. CONCLUSIONS: Nanobacteria may be an important etiological factor for type III prostatitis.

Two-dose basiliximab compared with two-dose daclizumab in renal transplantation: a clinical study.

BACKGROUND: Addition of the interleukin-2 receptor (IL-2R) antagonists basiliximab or daclizumab to a calcineurin inhibitor-based regimen significantly reduces risk of acute rejection with a tolerability profile similar to a placebo. Use of a truncated two-dose regimen of daclizumab has been reported, but till date, there has been no controlled study of two-dose daclizumab vs. two-dose basiliximab. METHODS: Deceased-donor renal transplant recipients were randomized to basiliximab (20 mg on days 0 and 4) or daclizumab (50 mg on days 1 and 14) with cyclosporine, mycophenolate mofetil and corticosteroids. Flow cytometry was used to calculate the proportion of CD25(+) T cells in peripheral blood. RESULTS: Thirty patients were randomized to basiliximab and 28 to daclizumab. There was one patient death in each group, with no other graft losses. By six months, the incidence of biopsy-proven acute rejection was 0% with basiliximab vs. 21.4% with daclizumab (p < 0.05). Three patients in the daclizumab group required OKT3 for steroid-resistant rejection. There were no between-group differences in the incidence of infection. The proportion of CD25(+) T cells declined markedly during the first two wk in both groups, but was significantly lower in the basiliximab group during weeks six to eight. CONCLUSION: Two doses of basiliximab are more effective than two 1 mg/kg doses of daclizumab in preventing acute rejection in de novo renal transplant patients receiving cyclosporine, mycophenolate mofetil and corticosteroid maintenance therapy. In patients receiving relatively low-level immunosuppression in order to minimize toxicity, basiliximab may be preferable to a truncated daclizumab regimen.