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Osteoporosis （OP） is a systemic metabolic bone disease. Amid population aging， OP has become a major health problem for the middle-aged and the elderly in China. Aging， iron load， and estrogen deficiency break the balance between oxidation and antioxidant systems， and the increase of reactive oxygen species mediates oxidative stress to damage DNA， lipids， proteins and other macromolecules， thus accelerating cell apoptosis and inducing OP， obesity， and neurodegenerative disorders. It has been found that oxidative stress is of great significance in the pathogenesis of OP. Oxidative stress regulates the signaling pathways， cytokines， and proteins related to the mesenchymal stem cells， osteoblasts， and osteoclasts， thereby weakening the osteogenic differentiation of mesenchymal stem cells， inhibiting osteoblast mineralization， and promoting the activation， proliferation， and maturation of osteoclasts. As a result， the dynamic imbalance between bone resorption and bone formation occurs， influencing bone remodeling and promoting the progression of OP. At the moment， anti-bone resorption drugs， bone formation-promoting drugs， and hormones are mainly used in clinical settings in western medicine. However， due to the long treatment cycle and the occurrence of serious gastrointestinal reactions， hypocalcemia， osteonecrosis， and others， patients show poor compliance and thus the effect is not as expected. Traditional Chinese medicine （TCM） demonstrates remarkable effect on OP attributing to the multi-pathway and multi-target characteristics. With low price and few adverse reactions， TCM is widely applied in clinical practice in comparison with western medicine. TCM has unique advantages in the treatment of OP by regulating oxidative stress. It exerts the therapeutic effect on OP by modulating different signaling pathways， providing new mindset for the treatment of this disease. Therefore， through literature research， this study summarized the research on mechanism of oxidative stress in OP and the treatment by TCM， which is expected to lay a foundation for further research.
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Objective To study the effect of non-self-similar hierarchy on fracture mechanical properties and crack propagation of the biocomposite. Methods The numerical models were established by using ABAQUS, and the stiffness and crack initiation and propagation in the biocomposite with the inclination angles between the axis of the prism and mineralized collagen fibrils θ=0°,20°,40°,60°,80° were simulated by extended finite element method. Results The inclination angle θ had limited influences on biocomposite stiffness at θ≤40°, while biocomposite stiffness decreased with θ at θ>40°. The ultimate tensile strain also increased at θ>40°. Asymmetry in the crack was also found during propagation of matrix surrounded-enhanced phases at θ>0°. The crack propagatation on one side of the long axis of the mineral crystal was relatively easier than that on the other side at θ>0°. Conclusions The non-uniform distributions of cracks were found in biological hard tissues arisen from the non-self-similar hierarchy. The non-uniform crystal arrangement in the biocomposite would result in local damage rather than catastrophic fracture. The findings of this study can provide theoretical support for material design.
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Objective To compare the pressure-controlled ventilation (PCV) and volume-controlled ventilation (VCV) in the patients undergoing spinal surgery in prone position supported by a Wilson frame.Methods Forty patients,of ASA physical status Ⅰ or Ⅱ,aged 30-64 yr,with body mass index ＜ 30 kg/m2,scheduled for elective spinal surgery in prone position supported by a Wilson frame under general anesthesia,were randomly allocated to receive mechanical ventilation using either VCV (n =20) or PCV (n =20) mode.Endotracheal intubation and mechanical ventilation were performed after induction of anesthesia.The tidal volume (VT) was set at 10 ml/kg according to the ideal body weight in group VCV.The maximal inspiratory pressure of the anesthesia machine was adjusted to maintain the VT at 10 ml/kg in group P.Both ventilation modes were required to maintain PET CO2 within the normal range.VT,respiratory rate,minute ventilation (MV),dynamic lung compliance (Cdyn),peak and mean airway pressure (Ppeak,Pmean),mean arterial pressure (MAP) and HR were recorded at 10 min after the patients were turned to supine position and at 30 min after the patients were turned to prone position after intubation.Arterial blood samples were collected for blood gas analysis,and oxygenation index(OI) and physiologic dead space fraction (VD/VT) were calculated.Results Compared with those at 10 min after turning to supine position,Ppeak was significantly increased and Cdyn,VT and MV were decreased at 30 min after turning to prone position in both groups.Compared with group VCV,Ppeak was significantly decreased,respiratory rate and Cdyn were increased,and no significant change was found in VT,MV,OI,VD/VT,Pmean,MAP and HR in PCV group.Conclusion Compared with VCV,PCV can improve the ventilatory efficacy and reduce the influence of prone position on respiratory dynamics in the patients undergoing spinal surgery in prone position supported by a Wilson frame.
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BACKGROUND: The molecular mechanism and core regulatory network of deep vein thrombosis are not fully clarified yet.OBJECTIVE: To explore the roles of oxidative stress and Rac1/2 in rat deep vein thrombosis.METHODS: Deep vein thrombosis model in SD rats was established by a champing method femoral veins clamping combinedwith fixation of the lower extremity with plaster. The incidence and serious degree of thrombus were observed by dissecting ratfemoral vein at different time points (2.5 and 25 hours after modeling). The model rats were divided into pre-thrombogenesisgroup (2.5 hours after modeling), thrombogenesis group (25 hours after modeling) and non-thrombogenesis group (25 hours aftermodeling). Then total RNA and protein were extracted from the femoral venous wall tissues.RESULTS AND CONCLUSION: Colorimetry results showed that compared with the non-thrombogenesis group, theconcentration of malondiadehyde in rat femoral vein wall tissues of the thrombogenesis group was the highest (P < 0.05), followedby that of the pre-thrombogenesis group (P < 0.05). The concentrations of total superoxide dismutase and glutathione reductasein the thrombogenesis group were the lowest, followed by those in the pre-thrombogenesis group (P < 0.05). The results of genechip hybridization analysis and real-time PCR showed that compared with the non-thrombogenesis group, the expressions ofRac1 and Rac2 in rat femoral vein wall tissues of thrombogenesis group increased the most, followed by that of thepre-thrombogenesis group (P < 0.05). These findings indicate that the up-regulation of malondialdehyde and Rac1/2 as well asthe activity decrease of total superoxide dismutase and glutathione reductase may lead to the formation of deep venousthrombosis.
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BACKGROUND: At present, the basic underlying molecular mechanism regulating the interactions among venous endothelial cells, platelets, leukocytes, and promoting local deep vein thrombosis microenvironment formation, still remains unclear, and there is no ideal method for early diagnosis of deep vein thrombosis. OBJECTIVE: To study the underlying role of nuclear factor kappa B1 and tissue factor in rats with deep vein thrombosis. METHODS: A total of 67 Sprague-Dawley rats were randomly divided into control group (n=10) and model group (n=57). Deep vein thrombosis model was established by a clamping and sewing method in femoral vein combined with cast fixation. The incidence and serious degree of thrombus were observed by dissecting rat femoral vein in different time points (2.5 and 25 hours after modeling). The model group was further divided into pre-thrombogenesis group (2.5 hours after modeling), thrombogenesis group (25 hours after modeling) and non-thrombogenesis group (25 hours after modeling). Then total RNA was extracted from the localized femoral venous endothelial tissue. The candidate genes, associated inflammation and thrombosis, were screened by a special gene chip. Then the gene expression of nuclear factor kappa B1 and tissue factor was further identified by real-time polymerase chain reaction. RESULTS AND CONCLUSION: Pre-thrombogenesis group had no thrombogenesis, while thrombogenesis group have 23 cases with thrombosis and non-thrombogenesis group have 22 cases without thrombosis. The results of gene chip hybridization analysis and real-time PCR found that the mRNA expression of nuclear factor kappa B1 and tissue factor in rat femoral vein endothelial tissue were significantly up-regulated at 2.5 hours after modeling (pre-thrombogenesis group was higher than control group) (P < 0.05), and continued up-regulating at 25 hours after modeling (thrombogenesis group was higher than the pre-thrombogenesis group, non-thrombogenesis group and control group) (P < 0.05). The results from present study indicate that up-regulating expressions of nuclear factor kappa B1 and tissue factor in local femoral venous endothelial tissue of rat deep vein thrombosis models may play a key role in initiating venous thrombosis.
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BACKGROUND: At present, the basic molecular etiological mechanism and core regulatory network of deep vein thrombosis (DVT) remains uncertain, and there is not an ideal measure for early diagnosis of DVT. OBJECTIVE: To study the underlying impact of cathepsin L/G in DVT rat model. METHODS: DVT rat models (n = 50) were established by clamping both femoral vein in three different positions within 3 seconds with mosquito forceps and fixing with cast. According to different observation phases and biological situations of the femoral vein thrombosis, model rats were divided into thrombogenesis group, pre-thrombogenesis group and non-thrombogenesis group. An additional 10 normal rats served as control group. Femoral vein was obtained at corresponding time points to exact total RNA. After a gene chip-based screening, the data of gene expression were further dissected by real-time PCR. RESULTS AND CONCLUSUON: Gene chip hybridization analysis results demonstrated that differential expression of cathepsin L/G gene was significant among groups, and the expression was greatest in the thrombogenesis group, followed by pre-thrombogenesis and non-thrombogenesis groups, which was significantly greater than the control group (P < 0.05). Real-time PCR analysis results were consistent with gene chip hybridization analysis results. These indicate that DVT is associated with an increase in expression of cathepsin L/G in local venous vascular wall, and they may be candidate molecular markers for early diagnosis of deep vein thrombosis.
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BACKGROUND:Studies in recent years have demonstrated that arginase Ⅰ contribute to the process of numerous cardiovascular diseases,however,most of studies focus on arteries,few regarding venous diseases.OBJECTIVE:To explore the changes of arginase Ⅰ expression in rat traumatic deep venous thrombosis models,and to analyze the possible function of arginase Ⅰ in deep venous thrombosis formation.METHODS:Totally 100 Sprague Dawley rats were randomly divided into the control and model groups.Traumatic deep venous thrombosis models were established by clamping the femoral vein and immobilizing the bilateral hind limbs (hip spica cast fixation),and assigned into initial thrombosis,peak thrombosis and non-thrombosis groups according to different observing time points and pathophysiological situations of thrombosis.Whole blood RNA of each group was extracted,and the change of arginase I expression in blood cells of each group was detected by real-time PCR.RESULTS AND CONCLUSUON:Expression of arginase Ⅰ in the peak thrombosis group was significantly increased compared with other 3 groups (P < 0.01).There were no significances among control,initial thrombosis and non-thrombosis groups (P > 0.05).The finding demonstrated that arginase Ⅰ is closely related to deep vein thrombosis formation.
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Objective To explore the effect and injury mechanism of reactive oxygen species (ROS) after spinal cord injury (SCI) through detecting the dynamic changes of malonyldialdehyed (MDA)content in spinal cord and observing neurocyte apoptosis and correlation apoptosis factor expression after SCI. Methods Totally 132 adult SD male rats were randomly divided into three groups: sham group, SCI group, methylprednisolone (MPSS) group. The SCI of SD rats was performed by Allen's weight dropping way to impact on the posteriors of spinal cord T_(10). The contents of MDA were determined by chromatometry, the expression of Caspase-3 and Bcl-2 family in the injured spinal cord was detected by immunohistochemical staining;Apoptotic cells were detected by using fluorometric terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (fluorometric TUNEL) staining. Results The content of MDA in the injured cord increased significantly after SCI;R3eached the peak at 6 hours and 3 days post-injury, then dropped down gradually, then was back to the normal level after 7 days. The number of TUNEL labeling positive cells of SCI group increased at 6 hours post-injury;R3eached the peak at 3 days, then dropped down gradually;Bcl-2, Bax protein began to increase at 6 hours post-injury;R3eached the peak at 5 days after injury, then dropped down gradually. Caspase-3 protein began to increase at 6 hours post-injury;R3eached the peak at 3 days after injury, then dropped down gradually. The content of MDA, the number of TUNEL labeling positive cells, the expression of Caspase-3 and Bax of MPSS group decreased significantly than that of SCI group at the same time;R3espectively, while Bcl-2 protein was up-regulated after administration of MPSS.Conclusion ROS could promote the expression of Caspase-3 and degrade the ratio of Bcl-2/Bax to induce apoptosis of neurocyte, which might play significantly role in the process of secondary SCI. In addition, MPSS exerts neuroprotective effects against ROS toxicity, which might be of importance and might contribute to their clinical efficacy for the treatment of SCI.
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ObjectiveIn order to investigate anti-ageing mechanisms of the notoginsenoside Rg1,we used Aβ_(1-42) and D-galactose to establish aging rat model. Methods Ninety rats were divided into three groups at random: sham group, model group, treatment group. Aging rat models were established by injecting peritoneally D-galactose (100 mg/kg) to the rats for 56 days and after 35 days aggregated Aβ_(1-42)(μg) was injected to the right lateral ventricle of rats. Meantime, rats were treated by intragastric administration the notoginsenoside Rg1. Then spatial memory of experimental rats was examined with the Morris water maze(MWM). The thiol antioxidants including glutathione reductase (GR) and glutathione peroxidase (GSH-Px) activities were examined by colorimetric method. The concentration of the pro-caspase-3 and Bcl-2 were examined by the immunohistochemistry and Western blotting method. Results In aging model rats escape latercies were significantly prolonged (P<0.05), while decreases were seen in the time of staying the third quadrants of platform, the number of crossing over a platform, the concentration of the GR, GSH-Px, and pro-caspase-3 as compared with the sham group(P<0.05). After treatment of the notoginsenoside Rg1, the aging model rats exhibited significant increases in the time of staying the third quadrants of platform, the number of crossing over a platform, the concentration of the GR, GSH-Px, and pro-caspase-3(P<0.05), while a decrease was observed in escape latercies as compared to control group(P<0.05). Moreover there was no significant difference in the expression of the Bcl-2(P>0.05). Conclusion The results from our study indicate that the notoginsenoside Rg1 could improve the oriented learning and memory capacity and prevent the neurodegeneration of central nervous systems in aging model rats by up-regulating the expression of the thiol antioxidants(including GR and GSH-Px) and resisting the cleavage of the pro-caspase-3.
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ObjectiveTo examine the protective effects of 17-β estradiol on the experimental model of spinal cord injury (SCI) rats. Methods One hundred and eighty male Sprague Dawley (SD) rats, after Allen' s model, SD rats were divided into three groups: the sham group, the acute spinal cord injury (control groups) and the acute spinal cord injury supplying with 17-β estradiol treatment group. SCI was made by Allen's weight dropping, impacting on the posteriors of spinal cord T10. The content of malonyldialdehyed (MDA), glutathione (GSH), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were determined by chromatometry. The expressions of Caspase-3 and Bcl-2 family in the injured spinal cord were detected by immunohistochemical staining. Results The BBB scores at each time point in 17-β estradiol treatment group were significantly higher than that in SCI group (P<0.05). The contents of GSH, SOD, GSH-Px and the expression of Bcl-2 protein at the majority of time point in 17-β estradiol treatment group were significantly higher than that in SCI group(P<0.05), however, the MDA, Caspase-3 and Bax were markedly decreased (P<0.05). Conclusions This study suggests that 17-β estradiol administration might prevent the cells from SCI-induced apoptosis by triggering to reduce the oxidative stress.