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Objective To study the effect of hydrogen on mitochondrial function in cerebral cortex after cerebral ischemia/reperfusion(I/R)injury in rats. Methods 48 male SD rats were randomly divided into sham operation group(sham group),brain I/R injury group(MOD group),hydrogen treatment group(H2group). 24 hours after reperfusion,the neurological deficit scoring was performed. The changes of mitochondrial membrane potential(△ψm),permeability openness(MPTP),ROS production rate and mitochondrial swelling were detected. Results Compared with the Sham group,neurological deficit score,MPTP openness,mitochondrial swelling degree and ROS production rate were increased in the MOD group(P<0.01),△ψm levels were reduced(P<0.01). Compared with the MOD group,the neurological deficit score,MPTP openness,mitochondrial swelling degree and ROS production rate were decreased in H2group(P<0.01),△ψm levels increased(P<0.01). Conclusions Simul-taneous intraperitoneal injection of pure hydrogen can reduce the generation of reactive oxygen species,protect the mitochondrial function of neuronal cells in the ischemic region after brain I/R,improvement the rat brain I/R after the neurological scoring.
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Objective: To construct an antibacterial peptide controlled release coating for percutaneous implant and to study its release and antibacterial properties. Methods: TiO2 nanotube specimens were prepared by anodizing. PDLLA was used as the retarder and HHC-36 as the antibacterial peptide, PDLLA-HHC-36 were loaded on TiO2 nanotube surface by solvent-casting technology. The surface form of the specimens was observed under SEM. Sustained release was analyzed by the release curves and the antibacterial effect was examined with inhibition zone test. Results: TiO2 nanotube specimens with 80-120 nm diameter were fabricated, the drug coating was observed under SEM. The drug loaded specimens showed 15 days sustained release in vitro and inhibition zone about 15 mm in diameter was found in the test for at least 10 days. Conclusion: TiO2 nanotube specimens with PDLLA-HHC-36 controlled release coating has sustained-release and antibacterial properties.
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Objective To investigate the effect of hydrogen on mitochondrial membrane potential during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Eighty-four healthy adult male SPF Sprague-Dawley rats,weighing 220-240 g,were divided into 3 groups (n=28 each) using a random number table:sham operation group (Sham group),I/R group and hydrogen group (H2 group).Focal cerebral I/R was produced by mid-cerebral artery occlusion in I/R and H2 groups.Hydrogen 10 ml/kg was intraperitoneally injected immediately after onset of reperfusion and at 12 h of reperfusion in group H2.Neurological deficit was scored at 24 h of reperfusion.The rats were then sacrificed and brain tissues in cortex were removed for microscopic examination of the pathological changes and for determination of cerebral infarct size (by TFC staining),nerve cell apoptosis (by TUNEL),mitochondrial membrane potential (by JC-1 staining) and expression of Bcl-2 and Bax (by Western blot).Apoptotic index (AI) was calculated.Results Compared with Sham group,the neurological deficit score,percentage of cerebral infarct size and AI were significantly increased,the mitochondrial membrane potential was decreased,Bax expression in brain tissues was up-regulated,and Bcl-2 expression in brain tissues was down-regulated in I/R and H2 groups (P＜0.05).Compared with I/R group,the neurological deficit score,percentage of cerebral infarct size and AI were significantly decreased,the mitochondrial membrane potential was increased,Bax expression in brain tissues was down-regulated,and Bcl-2 expression in brain tissues was up-regulated (P＜0.05),and the pathological changes of brain tissues were significantly attenuated in H2 group.Conclusion The mechanism by which hydrogen reduces focal cerebral I/R injury is related to decreasing dissipation of mitochondrial membrane potential and inhibiting nerve cell apoptosis in rats.
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Objective:To evaluate the clinical outcomes of implant-retained overdentures.Methods:57 patients treated by implant-retained overdentures were included.Parameters for peri-implant tissue conditions (e.g.peri-implant probing depth,plaque index,bleeding on probing,mucosal hyperplasia,peri-implant marginal bone loss) and prosthetic complications were examined and recorded.The precentage of satisfaction of the patients was assessed using the visual analog scale (VAS).Results:After an average follow-up of (48±11.3) months,the survival rate of the implants was 98.1%,the marginal bone loss was (1.38±0.74) mm.There was no statistically difference among the different attachment groups(bar,magnet and ball) regarding the peri-implant marginal bone loss or bleeding on probing(P>0.05).The peri-implant probing depth and plaque index in patients with magnet and ball attachments were lower than those in patients with bar attachments(P0.05),except that magnet and ball attachments were much easier to clean compared with bar attachments(P<0.05).Conclusion:Implant-retained overdenture is a successful and satisfactory treatment option for patients with edentulous jaw.The patients should been given regular clinical examinations to keep peri-implant tissue health and reduce the complications,especially those with bar attachments.
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Objective To investigate the effects of inhaling high concentration of hydrogen gas on the expressions of endoplasmic reticulum stress(ERS) related protein glucose regulated protein 78 (GRP78),Caspase-12 and the neural cell apoptosis and related proteins Bcl-2 and Bax in the rats with focal cerebral ischemia reperfusion(I/R) injury.Methods Seventy-two healthy SPF male Sprague-Dawley rats were selected and then randomly divided into the control group(Ⅰ:without any treatment),sham operation group (Ⅱ),cerebral IRI group (Ⅲ) and hydrogen gas treatment group (Ⅳ),18 cases in each group.Focal cerebral ischemia reperfusion injury (IRI) model was induced by using the suture-occluded method.The neurological deficits score (NDS) was assessed at 24 h after cerebral reperfusion in four groups.The cerebral infarction severity and size were detected by TTC staining and neuronal apoptosis of brain cortex were tested by TUNEL technique.The apoptosis index (AI) was calculated.Then the expressions of GRP78,Caspase-12,Bcl-2 and Bax were assessed by Western blot and immunohistochemistry.Results As compared with the group Ⅰ and Ⅱ,NDS score,cerebral infarction size,AI and the expressions of GRP78,Caspase-12 and Bax in cerebral cortex in the group Ⅲl and Ⅳ were significantly increased,while the expression of Bcl-2 in cerebral cortex was markedly decreased(P＜0.05);compared with the group Ⅲ,NDS score,brain infarction size,AI and the expression of Caspase-12 and Bax in cerebral cortex in the group Ⅳ were markedly decreased,while the expressions of GRP78 and Bcl-2 were dramatically increased (P＜0.05).Conclusion Inhaling high concentration of hydrogen gas has a certain protective effect on cerebral IRI in rats through increasing endoplasmic reticulum GRP78 protein expression after IRI and inhibiting Caspase-12 activation,thus inhibiting ERS and promoting the repair function of endoplasmic reticulum.
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Objective To investigate the role of phosphatidylinositol 3?kinase∕protein kinase B∕glycogen synthase kinase?3β ( PI3K∕Akt∕GSK?3β) signaling pathway in hydrogen?induced inhibition of neuronal ap?optosis induced by focal cerebral ischemia?reperfusion ( I∕R) in rats. Methods One hundred and twenty healthy adult male Sprague?Dawley rats, weighing 200-220 g, were divided into 5 groups ( n=24 each) u?sing a random number table: sham operation group ( group S); cerebral I∕R group ( group I∕R); hydrogen group (group H2); LY294002 (specific PI3K inhibitor) group (group LY); LY294002+hydrogen group ( group LY+H2 ) . Focal cerebral I∕R was induced by occlusion of the middle cerebral artery for 1 h followed by 24 h reperfusion. In H2 and H2+LY groups, the animals inhaled 67% H2+33% O2 for 2 h starting from onset of reperfusion, and then inhaled H2 for 2 h every 6 h. In LY and LY+ H2 groups, LY294002 ( 10 mmol∕L) 10 μl was injected into the lateral cerebral ventricle at 10 min before reperfusion. Neurologic defi?cit was evaluated and scored ( NDS) at 24 h of reperfusion. The rats were then sacrificed, and the brains were removed for measurement of the cerebral infarct size ( by TTC staining) and apoptosis in cortical neu?rons ( by TUNEL) and for determination of the expression of Akt in the ischemic cerebral cortex, phospho?rylated Akt ( p?Akt) , GSK?3β and phosphorylated GSK?3β ( p?GSK?3β) and Bcl?2 and Bax positive cell count in the ischemic cerebral cortex ( by immuno?histochemistry) . The apoptosis index ( AI) , p?Akt∕Akt ratio and p?GSK?3β∕GSK3?β ratio were calculated. Results Compared with group S, the NDS, cerebral infarct size, AI, p?Akt∕Akt ratio, p?GSK?3β∕GSK?3β ratio and Bax positive cell count were significantly increased, and the Bcl?2 positive cell count was significantly decreased in group I∕R ( P0?05) . Compared with group H2 , the NDS, cerebral infarct size, AI and Bax positive cell count were significantly increased, and the p?Akt∕Akt ratio, p?GSK?3β∕GSK?3βratio and Bcl?2 positive cell count were significantly decreased in group LY+H2 ( P<0?05) . Conclusion The mechanism by which hydrogen inhibits focal cerebral I∕R?induced neuronal apoptosis is associated with the activation of PI3K∕Akt∕GSK?3β signaling pathway in rats.
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Objective To investigate the effect of high concentration hydrogen gas on neurons in the rat hippocampus CA1 region during global cerebral ischemic/reperfusion injury (GCIR) Methods Four-vessel occlusion was used to establish rat model with GCIR injury. One hundred and five healthy male Sprague-Dawley rats were randomly divided into sham operation group(SH group, n = 15), model group(4-VO group, n = 45) and treatment group(4-VO+H2 group,n = 45). After 72 h and 9 d reperfusion, hippocampal CA1 region pyramidal neurons in every group were detected with Nissle staining , immunohistochemical neuron-specific nuclear protein (NeuN), specific protein antibody microglial cells (Iba1) staining and the relationship of position between neurons and microglia was observed through fluorescence double staining. We used Morris water maze to test the space orientation ability and the learning and memory ability in rats after 9 d reperfusion. Results Compared with those of 4-VO group,the neurons of hippocampus CA1 region were closer to normal in 72 h and 9 d in 4-VO+H2 group and neuron form and the number of neuron survival were increased significantly (P < 0.05);immunohistochemical staining showed that the number of neuron survival in 4-VO+H 2 group was obviously higher than that in 4-VO group (P < 0.05) and the number of microglia in 4-VO group was obviously higher than that in 4-VO+H2 group (P < 0.05). Water maze experiment showed that the swimming time in quadrant Ⅳ in 4-VO+H2 group was longer than that in 4-VO group (P < 0.05). Conclusion Inhalation of high concentration hydrogen gas has prominent protective effect on neurons of rat hippocampal CA1 region during reperfusion. The mechanism may be related with inhibiting the microglia excitation and activation during GCIR.