Aim To study the effects of Procyanidins (PC) on apoptosis of PC12 cells induced by A? 25-35. Methods Cell survival rate was evaluated by MTT assay, and apoptosis was analyzed by Hoechst-PI fluorescence staining. The expressions of mRNA and protein for P53 and Bcl-2 were tested by RT-PCR and Western blot. Results Pretreatment with different concentrations of PC (10~30 mg?L -1) for 1h increased the survival rate of PC12 cells in a dose-dependent fashion. PC prevented the PC12 cells nuclei from shrinkage, condensation and cleavage induced by A? 25-35. PC decreased the expressions of P53 mRNA and P53 protein, and increased the expression of bcl-2 mRNA and Bcl-2 protein. Conclusion These results indicated that PC can protect PC12 cells from apoptosis induced by A? 25-35. The mechanism of protection is likely related to decreasing P53 gene expression, and increasing bcl-2 gene expression.

Objective To study the effect of procyanidins (PC) on mRNA and protein expression of par-4 and bcl-2 genes in PC12 cells induced by A?_ 25-35 . Methods Cell survival rate was evaluated by MTT assay and apoptosis was analyzed by Hoechst 33258-PI fluorescence staining. The expressions of mRNA and protein for par-4 and bcl-2 were tested by RT-PCR and Western blotting. Results Pretreatment with different concentrations of PC (5、10、20, and 30 mg/L) for 1 h increased the survival rate of PC12 cell in a dose-dependent manner. PC prevented the PC12 cells nuclei from shrinkage, condensation, and cleavage induced by A?_ 25-35 . PC decreased the expression of par-4 mRNA and protein, and increased the expression of bcl-2 mRNA and protein. Conclusion PC can protect PC12 cells from apoptosis induced by A?_ 25-35 in a dose dependent manner. The mechanism of protection is likely related to decreasing the par-4 gene expression and increasing the bcl-2 gene expression.

AIM: To investigate the effect of recombinant human interleukin-10 (rhIL-10) on IL-6 and TNF-? levels in serum and liver of mice exposed to lipopolysaccharide (LPS). METHODS: rhIL-10 was prepared by using genetic engineering technology. Mice were intraperitoneally with 500 ?g of LPS, and then were treated intravenously with various dosages of rhIL-10. The levels of IL-6 and TNF-? in hepatic tissue and serum were determined by ELISA at 12 h, 24 h, 48 h and 72 h post rhIL-10 treatment. RESULTS: rhIL-10 markedly inhibited the increase in IL-6 and TNF-? levels in hepatic tissue and serum at 12 h after rhIL-10 treatment in LPS-challenged mice, and the inhibition effect was significant at 24-48 h after rhIL-10 treatment (P