Recent studies show that epileptic seizures result in mass free radical production and induce oxidative damage because of relative deficiency in anti-oxygen system.Mitochondrium is crucial to sustaining energy metabolism,regulating cell death,synthesising neurotransmitter and oxidating fatty acid.Mitochondrium is not only the place for free radical production,but also the target of oxidative damage.Mitochondrial oxidative stress and resultant dysfunction enhance epileptic susceptibility.Seizure-induced free radical can influence energy metabolism,destroy DNA construction and induce apoptosis in neurontoxic consequences in epilepsy.

In order to explore the therapeutic action and mechanisms of Chang An Capsules for treatment of ulcerative colitis, 62 cases were randomly divided into two groups and treated with oral administration of Chang An Capsules and Bu Pi Yi Chang Pill respectively, for 3 therapeutic courses. Clinical observation, pathological therapeutic effects, and changes of enteroscopic sign , serum immunoglobin, complement C3, serum superoxide dismutase (SOD) and lipid peroxide (LPO) before and after treatment were observed. Results indicated that in the treatment group, the total effective rate was 93. 80%, the therapeutic effects for enteroscopy and pathology were 81. 30% and 84. 40% respectively, and serum immunoglobin, complement Cs, serum superoxide dismutase (SOD) activity and lipid peroxide (LPO) were improved or inhibited, with significant difference compared with the control group (P

OBJECTIVE:To investigate the role of interferon to increase the sensibilization of MGMT positive glioma stem cel s to temozolomide in vitro. METHODS:Glioma cel lines, U251 and SKMG-4, were induced by suspended cloning bal formation method to harvest MGMT positive glioma stem cel s, U251G and SKMG-4G. Cel counting kit-8 assay was used to detect the kil ing effect of interferonα/βcombined with temozolomide on MGMT positive glioma stem cel s. RT-PCR and western blot assay were employed to determine the expression of MGMT and nuclear factorκB in MGMT positive glioma stem cel s. RESULTS AND CONCLUSION:Western blot results showed positive expression of MGMT in U251G and SKMG-4G cel s at protein levels. After intervention with interferonα/β, the mRNA expression of MGMT and nuclear factorκB in SKMG-4G and U251G cel s was reduced significantly, and then further decreased after temozolomide treatment. These findings indicate that interferonα/βcan remarkably strengthen the kil ing effect of temozolomide on MGMT positive glioma stem cel s.

Lithium carbonate could be used to treat or prevent brain damage following traumatic injury and neurodegenerative diseases.It has been shown that its protective effect is related to protein kinase C (PKC) and extracellular signal-related kinase (ERK).It was demonstrated that PDBu,a PKC activator,inhibited amplitudes of delayed rectifier potassium current (It,) and produced a hyperpolarizing shift in the activation-voltage curve.The responses to PDBu were inhibited by lithium carbonate (50μmol/L).Further studies showed that when pretreated with MEK/ERK inhibitor U0126 (20 μmol/L),although PDBu significantly reduced IK,lithium did not reverse the effect of PDBu.Thus,the results suggested that PKC signaling cascades,along with MAPK (mitogen-activated protein kinase) pathway,were required in the phosphorylation of potassium channel,which was presented by regulation of potassium channel characteristic.AC-cAMP and their eross-talk with GC-cGMP pathway could also modulate the effect of lithium on PKC activation,which could be one of underlying mechanisms likely related to neuroprotective effect of lithium.

Objective To investigate the effects of nerve growth factor (NGF) on retinal synaptic plasticity of diabetic mellitus rat and its underlying mechanisms.Methods A total of 24 clean SD male rats were randomly divided into three groups (n =8),and they were control group,diabetic group and treatment group.In the latter two groups,a model of diabetic rats was induced by streptozotocin,and then the rats of treatment group were injected intraperitoneally 800 U · kg-1 NGF once a day after the model was induced successfully.Both control group and diabetic group were given the same amount of normal saline.Twelve weeks later,MDA content and SOD activity were detected;meanwhile,the expression of retinal synaptophysin was detected by immunofluorescence,and the expressions of retina synaptophysin and Caspase-3 were detected by Western blot.Results The difference of MDA content in the three groups was statistically significant (F =85.46,P ＜ 0.01);and the content of MDA in the diabetic group was significantly higher than that in the control group (P ＜0.01),while its content in the treatment group was significantly lower than that in the diabetic group (P ＜0.01).The difference of SOD activity in the three groups was statistically significant (F =17.76,P ＜0.01);and the SOD activity in the diabetic group was significantly lower than that in the control group (P ＜0.01),while its activity in the treatment group was significantly higher than that in the diabetic group (P ＜0.01).The difference of immunofluorescence intensity of synaptophysin in the three groups was statistically significant (F =395.42,P ＜ 0.01);immunofluorescence intensity of synaptophysin in the diabetic group was attenuated compared with the control group (P ＜0.01),while the intensity in the treatment group was enhanced compared with the diabetic group(P ＜0.01).The difference of the relative expression of synaptophysin in the three groups was statistically significant (F =17.27,P ＜ 0.01);and the expression of synaptophysin in the diabetic group was significantly downregulated compared with the control group (P ＜ 0.01),while its expression in the treatment group was upregulated compared with the diabetic group (P ＜ 0.01).The difference of relative expression of Caspase 3 protein in the three groups was statistically significant (F=217.13,P ＜0.01);and the expression level of Caspase 3 in the diabetic group was significantly higher than that in the control group (P ＜0.01),while its level in the treatment group was significantly lower than that in the diabetic group (P ＜ 0.01).Conclusion NGF can help to inhibit the apoptosis of retinal cell,restore the number of retina synapse by reducing the oxidative stress in diabetic retina,which suggests that NGF may be involved in the changes of synaptic plasticity in diabetic retina via oxidative stress pathway.

Objective To investigate the effects of inhibiting NgR on retinal ganglion cells density and synaptophysin expression of diabetic rat.Methods Thirty-two SD male rats were randomly divided into normal control group,diabetic group,siNgR group and scNgR group,8 rats in each group.Normal control group was given no any treatment.Diabetes model was induced by intraperitoneal injection of 50 mg · kg-1 streptozotocin in diabetic group,siNgR group and scNgR group,and the blood giucose more than 16.7 mmol · L-1 at 72 hours was set as the successfully model.The rats of siNgR group were intravitreally administrated with anti-NgR nucleotide and the rats of scNgR group intravitreally administrated with negative nucleotide.Eight weeks later,HE staining was conducted to detect density of retinal ganglion cell (RGC),immunofluorescence was used to evaluate the expression and distribution of synaptophysin (a marker of synaptic number).Relative expression of NgR and synaptophysin in retina were analyzed by Western blot.Results RGC density in normal control group,diabetes group,siNgR group and scNgR group were (624.33 ± 3.51) mm-2,(420.00 ± 2.65) mm-2,(621.67 ± 1.53) mm-2,(416.67 ± 2.52) mm-2,respectively.There was significant difference among four groups (F =5985.37,P ＜ 0.01).Compared with normal control group,RGC density in diabetes group and scNgR group were obviously decreased (all P ＜0.01),but siNgR group had no obviously change (P ＞ 0.05).The synaptophysin mainly expressed in the inner and outer network layer.Compared with normal control group,the positive expression of synaptophysin in diabetes group and scNgR group were decreased,but siNgR group had no obviously change.The relative expression of NgR in normal control group,diabetes group,siNgR group and scNgR group were (11.26 ±0.02) ％,(19.38 ± 0.10) ％,(11.17 ± 0.02) ％,(19.47 ± 0.31) ％,respectively.There was significant difference among four groups (F =2466.09,P ＜ 0.01).Compared with normal control group,the relative expression of NgR in diabetes group and scNgR group were obviously decreased (all P ＜ 0.01),but siNgR group had no obviously change (P ＞0.05).The relative expression of synaptophysin in normal control group,diabetes group,siNgR group and scNgR group were (35.76 ± 0.15) ％,(25.47 ± 0.36) ％,(35.28 ± 0.12) ％,(25.03 ± 0.75) ％,respectively.There was significant difference among four groups (F =583.70,P ＜ 0.01).Compared with the normal control group,the expression of synaptophysin in diabetic group and scNgR group were decreased increased (all P ＜ 0.01),while there was no significant difference in siNgR group (P ＞ 0.05).Conclusion Inhibiting the expression of NgR in the retina of diabetic rats can help to restore the number of synapses and protect the damaged RGC.

Objective Comparison of induction time on the proliferation of induced adipose-derived stem cells (ADSC) to differentiate into Schwann-like cells (iSC).Methods From March,2017 to October,2018,ADSCs were isolated from inguinal adipose tissue of healthy adult female SD rats.Flow cytometry was performed to detect ADSC positive markers CD29,CD90 and negative marker CD45.iSC induction medium was used to culture ADSC.S-100 and GFAP were detected by immunofluorescence staining to confirm that ADSC had differentiated into iSC.Morphological changes of cells were observed by inverted microscope on day 1st,4th,7th,10th,13rd,16th and 19th after induction.MTS assay was used to evaluate cell proliferation ability.Tunel staining was applied to assess cell apoptosis.Results Both S100 and GFAP were expressed in iSC.On day 7th,the cell proliferation rate was significantly slower than that before induction (A value was 0.330±0.020 vs.0.400±0.004,P＜0.05).It was negatively correlated with induction time.On day 19th,the proliferation rate of iSC was lower than 50％ of the proliferation rate before induction (A value was 0.016±0.003 vs.0.400±0.004,P＜0.05).Apoptosis of iSC was more obvious than ADSC at the same time point.Conclusion The proliferation ability of ADSC-induced iSC is optimal within 7 days after induction.

Objective To observe the morphological structures of WHBE rabbit brain in vivo based on 3.0 T magnetic resonance imaging system (MRI), accumulate the basic biological data of WHBE rabbit brain imaging, and provide a background information to further expand the WHBE rabbit application.Methods Nine healthy adult male WHBE rabbits were intravenously anesthetized with 3% pentobarbital sodium.3.0 T MRI plus rabbit brain dedicated coil was used to perform routine transverse and sagittal scans, and the size of brain structures were measured.Results MRI scanning can be successfully performed to obtain sagittal and transverse T2WI or T1WI images of WHBE rabbit brain in vivo, and can be clearly observed the basic structures of WHBE rabbit brains in vivo, such as olfactory bulb, cerebrum, cerebellum and pituitary gland.In addition, high signal was found in the hippocampus of the left and right temporal lobes in 4 rabbits with T2WI, but also low signal appeared in the corresponding regions in T1WI, and the others were not abnormal.Meanwhile, the reference data of frontal lobe, hippocampus, cerebrum, lateral ventricles, pituitary gland and other related anatomical structures were also obtained.Conclusions Using the 3.0 T magnetic resonance imaging system and rabbit brain coil,the morphological and anatomical structures of rabbit brain can be clearly observed, and the basic imaging data of WHBE rabbits brain have been established preliminarily.

Objective To observe the way of vascularization of acellular nerves and evaluate the enhanced vascularization of using COMP-Ang-1 into acellular nerve on bridging sciatic nerve gaps by radiography.Methods From March,2013 to June,2014,acellular nerves were harvested by chemical extraction.Thirty-six female rats weighing 200-250 g were randomly divided into 2 groups:18 animals with 1 cm long sciatic nerve lesions were repaired by nerve grafting (control group),18 animals with 1 cm long sciatic nerve lesions were repaired by nerve grafting and COMP-Ang-1 were administrated after surgery.Grafts were harvested after perfusion of lead oxide (carotid artery) on day 7,day 14 and day 21 postoperatively.Radiography was performed to capture the two dimensional image.The rules of vascularization of acellular nerve and the enhanced effects of COMP-Ang-1 on vascularization were evaluated.Results The density of vessels in COMP-Ang-1 group were higher than control group after 7 days (2701.60 ± 318.93 vs.925.40 ± 106.22,P =0.030),14 days (3309.21 ± 381.31 vs.2832.70 ± 189.23,P =0.210) and 21 days (4787.33 ± 251.09 vs.3469.36 ± 232.10,P =0.030) postoperatively; the area of vessels in COMP-Ang-1 group were higher than control group after 7 days (9231.03 ± 581.91 μm2 vs.4839.01 ± 101.01 μm2,P =0.043) and 14 days (15561.13 ± 697.73 vs.6811.07 ± 250.05,P =0.049) postoperatively.Conclusion COMP-Ang-1 can enhance the vascularization of acellular nerves fairly.

Objective To observe the effect of JLP on transdifferentiation of human renal proximal tubular epithelial cells (HK-2),and to investigate the role of p38 MAPK signaling pathway in this process.Methods The knock-down plasmids of JLP were constructed.HK-2 cells were randomly divided into four groups:negative control cells (Ctrl-shRNA group),knock-down jlp cells (jlpshRNA group),negative control cells with FGF-2 treatment (FGF-2 group) and knock-down jlp cells with FGF-2 treatment(jlp-shRNA +FGF-2 group).The expressions of JLP,E-cadherin,TGF-β1,α-SMA,p-p38 MAPK protein were detected by Western blotting.After the induction of FGF-2 for 24 hours,the expressions of α-SMA,COL-Ⅰ,FN were detected by immunocytochemistry.Results Compared with Ctrl-shRNA group,the expression of JLP protein was significantly down-regulated in FGF-2 group.Compared with FGF-2 group,the expressions of TGF-β1,α-SMA,p-p38 MAPK protein were significantly up-regulated,while E-cadherin protein was significantly down-regulated (P ＜ 0.05).Compared with FGF-2 group,the expressions of α-SMA,COL-Ⅰ,FN immunostaining increased markedly in jlp-shRNA+FGF-2 group.Conclusion Scaffolding protein JLP is critical in preventing EMT in the course of fibrosis through the inhibition of p-p38 activation in HK-2 cells.