Ease in Bax expression in spinal cord. In addition, TMP significantly reduced the number of TUNEL-positive cells in anterior horn of the spinal cord, and the Bax/Bcl-2 expression appeared to correlate with the anti-apoptotic effect.It has been suggested that neuronal apoptosis occurs concurrently with necrosis following spinal cord I/R and may contribute predominantly to delayed onset of neuronal cell death [22,23]. The major mechanism of I/R induced apoptosis is attributed to the ROS release. ROS induces apoptosis by causing DNA damage, oxidation of lipid membranes, and activation of the proteins responsible for apoptosis[24,25]. Among these apoptosis regulatory pro-Page 6 of(page number not for citation purposes)BMC Neuroscience 2006, 7:http://www.biomedcentral.com/1471-2202/7/Figure 6 Effects of TMP on Bax expression in spinal cord at the 48th hour reperfusion Effects of TMP on Bax expression in spinal cord at the 48th hour reperfusion. Immunohistochemical photomicrographs (magnification ?400) of anterior horn tissue stained for Bax protein in sham group (A), control group (B) and TMP group (C). Immunostaining was performed using a specific anti- Bax antibody and developed with stable DAB. The positive staining of Bax is presented by a brown color of cytoplasm. Figures are representative of 3 separate experiments with similar results.teins, the Bcl-2 family consists of both cell death promoters and cell death preventers. The ratio of anti- to proapoptotic molecules such as Bcl-2/Bax determines the response to a death signal. Indeed, the role of the Bcl-2 family in A-836339 web regulating apoptosis has been characterized in CNS ischemia[26,27]. In addition, over-expression of Bcl2 may play a protective role in neuropathological sequelae after CNS insults [28]. Recent studies have revealed that antioxidants attenuated ischemic neuronal apoptosis through Bcl-2 up-regulation parallel to Bax down-regulation [29]. TMP has been reported to attenuate oxidative damage and apoptosisboth in vitro and in vivo [30,31]. In the present study, treatment with TMP is related to an up-regulated level of the anti-apoptotic protein Bcl-2 and a down-regulated pro-apoptotic protein Bax, suggesting that TMP exhibit an inhibitory effect on apoptotic cell death due to spinal cord I/R through modulation of Bcl-2 family.ConclusionTMP shows a potent protection against spinal cord I/R injury in rabbit model, and reduces apoptotic cell death through Bcl-2 up-regulation parallel to Bax down-regulation.Figure 7 Effects of TMP on Bcl-2 expression in spinal cord at the 48th hour reperfusion Effects of TMP on Bcl-2 expression in spinal cord at the 48th hour reperfusion. Immunohistochemical photomicrographs (magnification ?400) of anterior horn tissue stained for Bcl-2 protein in sham group (A), control group (B) and TMP group (C). Immunostaining was performed using a specific anti- Bcl-2 antibody and developed with stable DAB. The positive staining of Bcl-2 is presented by a brown color of cytoplasm. Figures are representative of 3 separate experiments with similar results.Page 7 of(page number not for citation purposes)BMC Neuroscience 2006, 7:http://www.biomedcentral.com/1471-2202/7/FOD[3URWHLQ /HYHO RQWURO6KDPRQWUROFigure 8 Effect of TMP on expression of Bcl-2/Bax PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/25432023 proteins in spinal cord at the 48th hour reperfusion Effect of TMP on expression of Bcl-2/Bax proteins in spinal cord at the 48th hour reperfusion. Western analysis was carried out as described under Methods and the.