Objective To investigate the expression of the cytosolic phospholipase A2(c-PLA2),interleukin-1 beta(IL-1?),tissue inhibitor of matrix metalloproteinase-1(TMP-1) in rat brain after injury.Methods The model of traumatic brain injury originally described by Feeney was employed.The mRNA was analyzed by RT-PCR.Results The mRNA of cytosolic phospholipase A2 was increased at 2 hour and its peak was at 7 day.At 14 day,the level of cytosolic phosphalipase A2 mRNA was still in high level as compared to the control group.Likely,the enhancement expression of interleukin-1? was seen at the 1 hour and the peak time was from 5 to 8 hour.At 72 hour,it decreased to normal level.The expression of inhibitor of matrix metalloproteinase-1 was increased at the 2 hour,and the highest expression level was seen during 48 to72 hour.It came down to normal level at 14 day after injury.Conclusion The augment of the expression of the cytosolic phospholipase A2,interleukin-1? and tissue inhibitor of matrix metalloproteinase-1 following traumatic brain injury suggested that they participated in the pathogenesis of the traumatic brain injury,and may played roles in this pathophysiological process.

Tubulin has been shown to be an effective target for the development of cytotoxic agents against prostate cancer. Previously, we reported that Lx2-32c is an anti-tubulin agent with high binding affinity to tubulin. In this study, we investigated the potential of Lx2-32c to act as an effective cytotoxic agent in the treatment of prostate cancer. MTT assays showed that Lx2-32c was cytotoxic to all tested prostate cancer cell lines. The Lx2-32c-treated cells typically exhibited a rounded morphology associated with the onset of apoptosis, as evidenced by immunocytochemical staining. Human prostate cancer cell lines treated with Lx2-32c arrest in the G2/M phase of the cell cycle and the treatment is associated with an increased ratio of cells in the sub-G0/G1 phase as determined by flow cytometry. Furthermore, expression of the cleaved form of poly (ADP-ribose) polymerase in prostate cancer cell lines treated with Lx2-32c was shown by Western blotting assay. Xenograft implants of LNCaP and PC3-derived tumors in nude mice showed that Lx2-32c treatment significant inhibited tumor growth with effects equivalent to those of docetaxel. These findings demonstrate the potential of Lx2-32c as a candidate antitumor agent for the treatment of prostate cancer.