Objective To evaluate the neuroprotective benefits of histone deacetylases (HDAC)inhibitor MS-275 in rats with moderate traumatic brain injury (TBI).Methods Sixty-eight adult male SD rats were assigned to sham injury + placebo treatment (control group),TBI + placebo treatment (injury group),TBI + MS-275 (15 mg/kg) treatment (treatment group Ⅰ) and TBI + MS-275 (45 mg/kg)treatment (treatment group Ⅱ) according to the random number table.An experimental model of moderate TBI in the rat was induced using a lateral fluid percussion device.MS-275 was dissolved in DMSO and administered (15 and 45 mg/kg) intraperitoneally in seven consecutive days(once a day).The first administration was done in 30 minutes postinjury.Alteration in body weight of rats in each group was recorded after injury.Spatial learning and memory retention in rats was assessed using the Morris Water Maze in days 10-14 after TBI.Brain tissues were sectioned to measure acetyl-histone H3 and neuronal survivals in the hippocampus CA2-3 region using immunohistochemistry and cresyl-violet staining techniques.Results TBI rats showed significant body weight loss in 3 days postinjury as compared with the controls (P ＜0.05) and then gradually gained the body weight in 4-5 days postinjury.No significant difference in actual body weight loss after injury was found among injury group and treatment groups (F =0.149,P ＞0.05).Behavioral result revealed that the animals in treatment groups had significant improvement in cognitive performance as compared with injury group (P ＜ 0.01).Immunohistochemical results presented a markedly increased level of acetyl-histone H3 in both treatment groups,with no significant difference as compared with control group and a trend of increase in the survived neurons in the CA2-3 hippocampus in 14 days postinjury (P ＞ 0.05).Conclusions MS-275 achieves visible improvement of acetyl-histone H3 level and cognitive performance in the acute phase of TBI.Simultaneously,this treatment has an ameliorative effect on pathological changes associated with TBI as well and provides a neuroprotective effect against TBI.

A resonance light scattering(RLS) method for the determination of critical micelle concentration(CMC) of sodium dodecyl benzene sulfonate(SDBS) was proposed. Under room temperature, the RLS intensity of the SDBS system increased with increasing SDBS concentration. And when the concentration of SDBS approached CMC, the RLS intensity had increased sharply. The RLS peaks were appeared at 330 nm and 396 nm, respectively. The plot of the RLS intensity at 396 nm versus SDBS concentration was S-Curve. The concentration of SDBS at the intersection point of two tangents to S-curve was considered as SBDS CMC. This result was consistent with the results of the pyrene probe fluorescence spectrometry and electrical conductivity method. The influences of the concentration of Ca2+ on the aggregation behave of SDBS and SDBS-emulsion OP(OP) systems were studied by the RLS method. The results indicated that the mixed

BACKGROUND:The method of ligating or resecting rat lower limb femoral or iliac artery has been widely used to make rat models of lower limb ischemia, but there have been no stable and efective methods used to establish diabetic models of chronic atherosclerotic occlusive diseases and to evaluate the ischemic status of hindlimbs of models. OBJECTIVE: To establish type 2 diabetes rat models of lower limb ischemia by feeding with high-fat diet and to evaluate them. METHODS:Twenty rats were randomly and evenly divided into diabetes group (n=10) and control group (n=10). Rats in the diabetes group were fed with high-fat diet for 6 months, and were intraperitonealy injected with streptozotocin (50 mg/kg) to induce diabetes. Rats in the control group were fed with normal diet for 6 months. Rats in these two groups were subjected to ligation of femoral artery to establish right lower limb ischemia models. RESULTS AND CONCLUSION:At the first day of modeling, color Doppler flow imaging and CT angiography showed obviously decreased blood flow suggesting the success of establishing ischemia model. At 7 and14 days after modeling, the blood flow of rats in these two groups showed a gradual recovery as detected by color Doppler flow imaging. At 28 days after modeling, blood flow of rats in the diabetes group was significantly slower than that in the control group (P < 0.05). CT angiography showed that at 28 days after modeling, only a smal amount of compensatory increase in blood flow of the blood vessels at the ligation position of proximal right lower limb femoral artery was seen in the diabetes group, while no obvious blow was observed in the distal part. Histopathologic and immunohistochemical staining showed that at 28 days after modeling, destroyed tissue structure and inflammatory cel infiltration were observed in the ischemic region and capilary density on the affected side was lower than that on the healthy side. The protein expression of vascular endothelial growth factor in the ischemic muscle tissue of rats in the diabetes group was significantly increased compared with that in the control group (P < 0.05). These results show that diabetic rat models of lower limb ischemia can be successfuly established by long term high-fat diet feeding and femoral artery ligation and they can be validated by CT angiography.