ABSTRACT
Objective To investigate the effect of probucol on Sertoli cell injury induced by oxygen-glucose deprivation/reoxygenation(OGD/R)and mechanism. Methods Primary Sertoli cells treated with oxygen glucose deprivation for 2 h and reoxygenation for 3 h were modeled. We incubated Sertoli cells with probucol in a concentration of 5,10,and 20 μmol/L from reoxygenation to the end. The cell viability was evaluated using Cell Proliferation Assay kit. ROS production was observed by flow cytometry. The levels of MDA ,iron and GSH or the activity of glutathione-dependent peroxidase were measured by Assay Kit. Results The ferroptosis inhibitors pre-vented cell death(P < 0.01). The cell death rate was decreased by probucol in time- and dose-dependent manner (P < 0.01). Meanwhile, probucol caused increase of ROS,MDA,GSH content and GPXs activity(P < 0.05). Conclusion Probucol protects Sertoli cells from OGD/R damage via inhibiting lipid peroxidation-mediated ferroptosis.
ABSTRACT
<p><b>OBJECTIVE</b>To construct a three-dimensional finite element model of the upper airway and adjacent structure of an obstructive sleep apnea hypopnea syndrome (OSAHS) patient for biomechanical analysis. And to study the influence of glossopharyngeum of an OSAHS patient with three-dimensional finite element model during titrated mandible advancement.</p><p><b>METHODS</b>DICOM format image information of an OSAHS patient's upper airway was obtained by thin-section CT scanning and digital image processing were utilized to construct a three-dimensional finite element model by Mimics 10.0, Imageware 10.0 and Ansys software. The changes and the law of glossopharyngeum were observed by biomechanics and morphology after loading with titrated mandible advancement.</p><p><b>RESULTS</b>A three-dimensional finite element model of the adjacent upper airway structure of OSAHS was established successfully. After loading, the transverse diameter of epiglottis tip of glossopharyngeum increased significantly, although the sagittal diameter decreased correspondingly. The principal stress was mainly distributed in anterior wall of the upper airway. The location of principal stress concentration did not change significantly with the increasing of distance. The stress of glossopharyngeum increased during titrated mandible advancement.</p><p><b>CONCLUSION</b>A more precise three-dimensional finite model of upper airway and adjacent structure of an OSAHS patient is established and improved efficiency by Mimics, Imageware and Ansys software. The glossopharyngeum of finite element model of OSAHS is analyzed by titrated mandible advancement and can effectively show the relationship between mandible advancement and the glossopharyngeum.</p>
Subject(s)
Humans , Finite Element Analysis , Mandible , Sleep Apnea, Obstructive , Tomography, X-Ray ComputedABSTRACT
Objective To study the effects of rehabilitation training on the expression of synaptophysin in the cortex after cerebral ischemia. Methods A model of focal cerebral ischemia was created in rats. The rats were divided into 4 groups at random 24 h after the cerebral ischemia was induced. The rehabilitation group was given bal-ancing, grasping, rotation, walking and other training every day. An immobilization group was fixed in their cages. The model control group and cerebral ischemia group were kept in general cages, taking food and moving freely. Im-munohistochemisty method was used to detect synaptophysin expression at the 1st, 7th, 14th, 21st and 28th day after the cerebral ischemia was induced. Results In the model control group, synaptophysin immunoreactive positive products were observed. In the cerebral ischemia group, the expression of synaptophysin decreased gradually. After rehabilitation training, synaptophysin immunoreactive positive products decreased slowly, but remained more abun-dant than among the immobilized rats. Conclusion After cerebral ischemia, the expression of synaptophysin de-creases. This demonstrates that the synaptic terminals were less injured. Rehabilitation training can enhance synapto-genesis in the cortex after cerebral ischemia.