Objective To explore the effect of NPY on activation of primary microglia and the production of in?terleukin-1β. Methods Rat primary cortical microglia was cultured and divided into control group, LPS group, NPY+LPS group, NPY group and BIBP3226+NPY+LPS group. Microglia in control group were incubated with serum-free me?dium for 6 h;microglia in LPS group were incubated with serum-free medium plus LPS for 6 h;microglia in NPY+LPS group were incubated with serum-free medium plus NPY and LPS for 6 h; microglia cells in NPY group were incubat?ed in serum-free medium plus NPY for 6 h; microglia cells in BIBP3226+NPY+LPS group were incubated in se?rum-free medium including BIBP3226 、NPY and LPS for 6 h. After 6 h , Primary cultured microglia were stained us?ing IBA-1 antibody and examined under the fluorescence microscope. The protein levels of IL-1βin the culture media and the mRNA expression levels of IL-1βin the microglia of different groups were detected using the methods of Elisa and RT-PCR. Results After 6 h, the contents of IL-1 βin the culture media and the mRNA expression levels of IL-1βin the cells of LPS group increased remarkably compared with control group (P<0.05) and the microglia were activat? ed. Compared with LPS group, the contents of IL-1 βin the culture media. the mRNA expression levels of IL-1β and the activity of microglia in LPS+NPY group were significantly decreased .Compared with LPS+NPY group, the contents of IL-1βin the culture media. the mRNA expression levels of IL-1β and the activity of microglia in BIBP3226+NPY+LPS group were increased (P<0.05). There were no significant differences in the contents of IL-1βin the culture media. the mRNA expression levels of IL-1βand the activity of microglia between BIBP3226+NPY+LPS group and LPS group or between NPY group and the control group. Conclusion NPY can inhibit the biological activity of microglia and IL-1βproduction through NPY Y1 receptorin the microglia.

Objective:To investigate the mechanism of crush syndrome (CS) induced by crush injury on myocardial cells in rats.Methods:Thirty two male Sprague Dawley (SD) rats were randomly divided into control group, CS-0 group, CS-12 group and CS-24 group with 8 rats in each group. CS model was made by self-made extruder and perfused with 4% paraformaldehyde for 0, 12 and 24 h. The morphological changes of myocardial tissue were observed by hematoxylin staining. The apoptosis of cardiomyocytes was detected by terminal dexynucleotide transferase-mediated nick end labeling (TUNEL). The levels and activities of malondialdehyde (MDA), superoxide dismutase (SOD), lactose dehydrogenase (LDH), interleukin-6 (IL-6), interleukin-1 β (IL-1 β), tumor necrosis factor-α (TNF- α) in myocardial homogenate were detected by enzyme-linked immunosorbent assay (ELISA). The expressions of Caspase-3, Bax, Bcl-2 and necrosis factor-κB (NF-κ B) were detected by Western blot.Results:Compared with the control group, the myocardial tissue of CS model group had different degrees of morphological damage; compared with the control group, the apoptosis rate, Caspase-3 and Bax protein expression levels of CS-0 group, CS-12 group and CS-24 group were significantly increased ( P<0.05), and the expression level of Bcl-2 protein was significantly decreased ( P<0.05); compared with the control group, the levels of MDA, LDH, IL-6, IL-1β, TNF-α and p65 protein phosphorylation in the myocardial homogenate of CS-0 group, CS-12 group and CS-24 group were significantly increased ( P<0.05), and SOD activity was significantly decreased ( P<0.05). Conclusions:CS may inhibit oxidative stress and induce inflammatory reaction by activating NF-κ B pathway, thus damaging myocardial cells in rats.