ABSTRACT
BACKGROUND: Edaravone, an effective free radical scavenger, has been reported to significantly improve the rehabilitation of limb locomotion after spinal cord injury (SCI), but the underlying mechanism remains unclear. OBJECTIVE: To explore the mechanism underlying edaravone promoting the recovery of limb locomotion in rats with SCI by observing the Basso, Beattie, Bresnahan scores and expression levels of collagen type I and IV. METHODS: Thirty-six rats were randomly allocated into three groups (n=12 per group): sham group (laminectomy plus intraperitoneal injection of normal saline), model group (SCI model by NYU impactor plus intraperitoneal injection of normal saline), and edaravone group (SCI model by NYU impactor plus intraperitoneal injection of edaravone). All rats were given the administration at the 1stday post-SCI for consecutive 7 days. The Basso, Beattie, Bresnahan scores were tested at 1, 3, 5 and 7 days post treatment. On day 7, all rats were sacrificed to remove the spinal cord, and the morphology of neurons in the spinal cord were observed by Nissl staining; the expression levels of collagen type I and IV were detected by immunohistochemistry and western blot assays. RESULTS AND CONCLUSION: Compared with the model group, the Basso, Beattie, Bresnahan scores in the edaravone group were significantly increased at day 5 post treatment (P < 0.05). Nissl staining showed a clear boundary between grey matter and white matter, and a large nucleolus in the neurocytoplasm in the sham group; there was a complete structure of neurons, slight cellular swelling and small hematoma area in the edaravone group; many and large cavitations and swollen nucleus were found in the neurons, even without nucleolus. Immunohistochemistry and western blot assay results showed that the expression levels of collagen type I and IV in the edaravone group were significantly higher than those in the model group (P < 0.05). These results indicate that edaravone can promote the recovery of limb locomotion of rats with SCI,probably via up-regulating the expression levels of collagen type I and IV.
ABSTRACT
<p><b>OBJECTIVE</b>To study the inhibitory effect of wogonin on the growth and proliferation of breast cancer cells MDA-MB-23, and observe its effect on the adhesion, migration and invasion of MDA-MB-23 cells, in order to further study its molecular mechanism.</p><p><b>METHOD</b>MTT assay was used to detect the effect of wogonin on MDA-MB-23 cell growth. Ki-67 assay was adopted to test the effect of wogonin on cell proliferation. Scratch test, adherence test and invasion chamber assay were taken to detect the effect on the migration and invasion abilities of MDA-MB-231 cells. Proliferation and metastasis-related proteins and relevant signaling pathways were detected by Western blotting.</p><p><b>RESULT</b>Wogonin could remarkably inhibit the growth and proliferation of MDA-MB-231 cells, significantly inhibit migration, adhesion and invasion abilities of breast cancer cells at a low concentration, and effectively inhibit the expression of Survivin, Bcl-2, ICAM-1, MMP-2, MMP-9 proteins of MDA-MB-231 cells.</p><p><b>CONCLUSION</b>Wogonin could notably inhibit growth and proliferation of breast cancer cells, and inhibit migration, adhesion and invasion of MDA-MB-231 cells. Its invasive and adhesive effects on MDA-MB-231 cells may be related to the decrease in ICAM-1, MMP-2, MMP-9 expressions.</p>