PubMed | General Hospital of Guangzhou Military Command, PLA Fourth Military Medical University, Fuzhou General Hospital of Nanjing Military Command and Xian No 4 Hospital
Type: | Journal: Oxidative medicine and cellular longevity | Year: 2016
Cytoprotectant amifostine attenuates radiation-induced oxidative injury by increasing intracellular manganese superoxide dismutase (SOD2) in peripheral tissue. However, whether amifostine could protect neuronal cells against oxidative injury has not been reported. The purpose of this study is to explore the protection of amifostine in PC12 cells.PC12 cells exposed to glutamate were used to mimic neuronal oxidative injury. SOD assay kit was taken to evaluate intracellular Cu/Zn SOD (SOD1) and SOD2 activities; western blot analysis and immunofluorescence staining were performed to investigate SOD2 protein expression; MTT, lactate dehydrogenase (LDH), release and cell morphology were used to evaluate cell injury degree, and apoptotic rate and cleaved caspase-3 expression were taken to assess apoptosis; mitochondrial superoxide production, intracellular reactive oxygen species (ROS), and glutathione (GSH) and catalase (CAT) levels were evaluated by reagent kits.Amifostine increased SOD2 activity and expression, decreased cell injury and apoptosis, reduced mitochondrial superoxide production and intracellular ROS generation, and restored intracellular GSH and CAT levels in PC12 cells exposed to glutamate. SOD2-siRNA, however, significantly reversed the amifostine-induced cytoprotective and antioxidative actions.SOD2 mediates amifostine-induced protection in PC12 cells exposed to glutamate.
Zhang L.,Xian No 4 Hospital
International Eye Science | Year: 2013
AIM: To evaluate the clinical feasibility of using a new optical coherence interferometry (IOL-Master), comparing with traditional ultrasonic biometry and manual keratometry in the accuracy and characteristics for intraocular lens calculation of high myopia. METHODS: The measurement of axial length was performed in 60 eyes (30 eyes for each group) with senile cataract of high myopia (≥-6.00D) using IOL-Master and ultrasonic biometry. The measurement of corneal power(K) was also performed in the patient using IOL-Master and manual keratometry preoperatively. Phacoemulsification and foldable lens implantation were done on the patients. IOL power calculation was carried out according to the SRK/T formula on the basis of the group-related data. Best corrected visual acuity, refraction, contrast sensitivity and wave front aberration root mean square (RMS) were re-tested after 3 months postoperatively. RESULTS: Significant difference between the two methods in axial length measurement which was 29.81±1.53mm by ultrasound and 29.63±1.81mm by IOL-Master (P=0.001). And in corneal power measurement which was 43.22±1.67K by manual keratometry and 44.27±1.39K by IOL-Master (P=0.006). There was a significant difference between the two groups (P=0.001). 63.0% vs 31.2% had a mean absolute refractive error (MARE) within ±0.50 diopter for the IOL-Master and A-scan groups, respectively (χ2=3.1, P<0.05). The RMS values of 4th order aberration, 4th order spherical aberration and total high order aberration in the IOL-Master group were lower than those in the A-scan group at 6mm pupil diameter 3 months later. CONCLUSION: IOL-Master is a non-contact, accurate, safe and reliable tool for calculating IOL power and it is more accurate on the design of the IOL in the cataract surgery on the high myopia patients.
Zhu Y.,Xi'an Jiaotong University |
Zhu Y.,Xian No 4 Hospital |
Zhang X.-L.,Xi'an Jiaotong University |
Zhu B.-F.,Xi'an Jiaotong University |
Ding Y.-N.,Xi'an Jiaotong University
Molecular Biology Reports | Year: 2012
Diabetic retinopathy (DR) is a leading cause of blindness globally and its pathogenesis has still not been completely elucidated. Some studies show a close relation between oxidative stress and DR. This study was aimed to investigate the effects of anti-oxidant in DR and expression of vascular endothelial growth factor (VEGF) and intercellular adhesion molecule-1 (ICAM-1) from retinal blood vessels in diabetic rats. Diabetic rat models were established by intraperitoneal injection of streptozotocin (60 mg/kg) and confirmation of high serum glucose levels in the animals. Antioxidant N-acetylcysteine was given to diabetic rats to elicit antioxidative responses, and rats were sacrificed at 3 and 5 months. Ultrastructures of retinal vascular tissues were observed under transmission electron microscope, and pathology of retinal capillaries was examined using retinal vascular digest preparations. Changes in the expression of VEGF and ICAM-1 were examined by immunofluorescence; and reactive oxygen species contents in the retinas were detected using dichlorofluorescein assay. Compared with normal rats, diabetic rats displayed significant retinopathy both under electronic and light microscopy, accompanied by elevated reactive oxygen species contents in the retinas; N-acetylcysteine treatment alleviated the pathological changes and also decreased reactive oxygen species, most significantly at 5 months. VEGF and ICAM-1 expressions were significantly up-regulated in retinal blood vessels from diabetic rats, and such up-regulation was attenuated by N-acetylcysteine treatment. The expression of both factors returned to basal levels after 5-month treatment with N-acetylcysteine. Long-term N-acetylcysteine treatment exerts protective effects on the diabetic retinas, possibly through its down-regulation of the expression of VEGF and ICAM-1, and reduction of reactive oxygen species content in retinal vascular tissues in diabetic rats. © Springer Science+Business Media B.V. 2011.
Ai H.,Xian No 4 Hospital |
Song H.-P.,Xian No 4 Hospital
International Journal of Ophthalmology | Year: 2012
AIM: To investigate the levels of serum soluble intercellular adhesion molecules-1(sICAM-1) and neutrophilic expression of CD18 in patients with various stages of diabetic retinopathy and to determine their different expression pattern in the development of diabetic retinopathy(DR). METHODS: Levels of serum sICAM-1 and CD18 on the surface of neutrophile were measured in 41 DR patients, they were classified in three subgroups according to the stage of retinopathy as determined by fund's ophthalmoscopy; 10 control subjects were also studied. sICAM-1 were measured by enzyme-linked immunosorbent assay and CD18 by flow cytometry. RESULTS: The neutrophilic CD18 expression and serum sICAM-1 level were all significantly elevated in all diabetic subgroups compared to control subjects (P<0.01). The differences of CD18 and sICAM-1 among the diabetic subgroups were significant in CD18 but not in sICAM-1. The progression of retinopathy was associated with an increase both in CD18 and in sICAM-1 levels by simple correlation analysis (β=0.74, P<0.001; β=0.38, P<0.01, respectively). But stepwise multiple regression analysis revealed that only CD18 was independent determinant of retinopathy (β=1.04, P<0.01). CONCLUSION: Our results confirm the contribution of endothelial and neutrophilic activation in the development of DR as indicated by increased levels of CD18 and sICAM-1. However, a direct implication of CD18 and ICAM-1 in the progression of DR can be supported only in the CD18 but not ICAM-1. CD18 and ICAM-1 may play different role in the development of diabetic retinopathy. Copyright International Journal of Ophthalmology Press.
Chen L.,Xian No 4 Hospital |
Yang X.-G.,Xian No 4 Hospital
International Journal of Ophthalmology | Year: 2011
AIM: To assess the impact of psychotherapy on psychology, visual field and intraocular pressure (IOP) in primary angle-closure glaucoma patients. METHODS: One hundred patients with primary angle-closure glaucoma took part in the survey. Symptom check list-90 (SCL-90), self-rating depression scale (SDS) and self-rating anxiety scale (SAS) were used. The visual field, IOP and HRT II were examined 3 months after operation. RESULTS: After psychotherapy, the score of depression, paranoid, anxiety, phobia in SCL-90 had changed significantly in therapy group. Compared with non-therapy group, the score of therapy group in SAS and SDS had altered, too. 3 months after operation, the IOP of therapy group was lower than that of non-therapy group, there was statistical significance. However, the MD and PSD had no change between two groups. In HRT II the differences about C/D and line C/D were obvious in two groups. CONCLUSION: Psychotherapy has some auxiliary effect for primary angle-closure glaucoma patients.
Zhang Z.-H.,Oak Ridge National Laboratory |
Chen H.,Northwest University, China |
Vaziri N.D.,University of California at Irvine |
Mao J.-R.,Affiliated Hospital of Shaanxi Institute of Traditional Chinese Medicine |
And 4 more authors.
Journal of Proteome Research | Year: 2016
Chronic kidney disease (CKD) has emerged as a major public health problem worldwide. It frequently progresses to end-stage renal disease, which is related to very high cost and mortality. Novel biomarkers can provide insight into the novel mechanism, facilitate early detection, and monitor progression of CKD and its response to therapeutic interventions. To identify potential biomarkers, we applied an UPLC-HDMS together with univariate and multivariate statistical analyses using plasma samples from patients with CKD of diverse etiologies (100 sera in discovery set and 120 sera in validation set) and two different rat models of CKD. Using comprehensive screening and validation workflow, we identified a panel of seven metabolites that were shared by all patients and animals regardless of the underlying cause of CKD. These included ricinoleic acid, stearic acid, cytosine, LPA(16:0), LPA(18:2), 3-methylhistidine, and argininic acid. The combination of these seven biomarkers enabled the discrimination of patients with CKD from healthy subjects with a sensitivity of 83.3% and a specificity of 96.7%. In addition, these biomarkers accurately reflected improvements in renal function in response to the therapeutic interventions. Our results indicated that the identified biomarkers may improve the diagnosis of CKD and provide a novel tool for monitoring of the progression of disease and response to treatment in CKD patients. © 2016 American Chemical Society.
Zhao Y.-Y.,Northwest University, China |
Zhang L.,Xian No 4 Hospital |
Feng Y.-L.,Northwest University, China |
Chen D.-Q.,Northwest University, China |
And 4 more authors.
Journal of Separation Science | Year: 2013
2,3,5,4′-Tetrahydroxystilbene-2-O-β-D-glucoside (THSG) from Polygoni multiflori has been demonstrated to possess a variety of pharmacological activities, including antioxidant, anti-inflammatory and hepatoprotective activities. Ultra-performance LC-quadrupole TOF-MS with MS Elevated Energy data collection technique and rapid resolution LC with diode array detection and ESI multistage MSn methods were developed for the pharmacokinetics, tissue distribution, metabolism, and excretion studies of THSG in rats following a single intravenous or oral dose. The three metabolites were identified by rapid resolution LC-MSn. The concentrations of the THSG in rat plasma, bile, urine, feces, or tissue samples were determined by ultra-performance LC-MS. The results showed that THSG was rapidly distributed and eliminated from rat plasma. After the intravenous administration, THSG was mainly distributing in the liver, heart, and lung. For the rat, the major distribution tissues after oral administration were heart, kidney, liver, and lung. There was no long-term storage of THSG in rat tissues. Total recoveries of THSG within 24 h were low (0.1% in bile, 0.007% in urine, and 0.063% in feces) and THSG was excreted mainly in the forms of metabolites, which may resulted from biotransformation in the liver. © 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
PubMed | University of Sichuan and Xian No 4 Hospital
Type: Comparative Study | Journal: Clinical therapeutics | Year: 2016
Retrospective, case-control studies and prospective randomized controlled trials (RCTs) on insulin treatment for diabetic patients yielded contradictory mortality and cardiovascular outcomes. We aimed to evaluate the effects of insulin versus oral hypoglycemic agents (OHAs) on all-cause mortality and cardiovascular outcomes in patients with type 2 diabetes (T2D).We searched Medline, Embase, Cochrane Central Register of Controlled Trials, Chinese Biological Medicine Database, China National Knowledge Infrastructure, Chinese Technical Periodicals, and Wanfang Data, up to July 10, 2015, for RCTs on insulin and OHAs that assessed all-cause mortality and/or cardiovascular death as primary end points. We derived pooled risk ratios (RRs) as summary statistics.Three trials were included in which 7649 patients received insulin and 8322 received OHAs, with mean (SD) diabetes duration of 5.0 (6.2) and 4.4 (5.9) years, respectively. Insulin did not differ from OHAs in all-cause mortality (RR = 1.00; 95% CI, 0.93-1.07), cardiovascular death (RR = 1.00; 95% CI, 0.91-1.09), myocardial infarction (RR = 1.04; 95% CI, 0.93-1.16), angina (RR = 0.97; 95% CI, 0.88-1.06), sudden death (RR = 1.02; 95% CI, 0.66-1.56), or stroke (RR = 1.01; 95% CI, 0.88-1.15). Insulin reduced the risk of heart failure compared with OHAs (RR = 0.87; 95% CI, 0.75-0.99). In the subgroup of secondary prevention of cardiovascular diseases (CVDs) or very high risk of CVDs, insulin did not differ from OHAs in all-cause mortality (RR = 0.99; 95% CI, 0.92-1.07), cardiovascular death (RR = 0.99; 95% CI, 0.90-1.09), myocardial infarction (RR = 1.01; 95% CI, 0.88-1.15), heart failure (RR = 0.69; 95% CI, 0.34-1.40), or stroke (RR = 1.05; 95% CI, 0.90-1.21).Insulin did not provide a clear benefit over OHAs in all-cause mortality or cardiovascular outcomes in the patients with T2D. Insulin therapy has many shortcomings, including inconvenience (injection, strict blood glucose monitoring), hypoglycemia, and obvious weight gain. Thus, we conclude that no robust evidence supports the active use of insulin for this population at present.
PubMed | Xi'an Jiaotong University and Xian No 4 Hospital
Type: | Journal: Molecular immunology | Year: 2016
Emerging evidence has indicated that vascular endothelial cells (ECs) not only form the barrier between blood and the vessel wall but also serve as conditional innate immune cells. Our previous study found that SIRT1, a class III histone deacetylase, inhibits the inflammatory response in ECs. Recent studies revealed that SIRT1 also participates in the modulation of immune responses. Although the NLRP3 inflammasome is known to be a crucial component of the innate immune system, there is no direct evidence demonstrating the anti-inflammatory effect of SIRT1 on ECs through the NLRP3 inflammasome. In this study, we observed that lipopolysaccharide (LPS) and adenosine triphosphate (ATP) triggered the activation of NLRP3 inflammasome in human umbilical vein ECs (HUVECs). Moreover, SIRT1 expression was reduced in HUVECs stimulated with LPS and ATP. SIRT1 activator inhibited the expression of monocyte chemotactic protein-1 (MCP-1) and C-reactive protein (CRP), whereas SIRT1 knockdown resulted in significant increases in MCP-1 and CRP levels in HUVECs stimulated with LPS and ATP. Importantly, the lack of SIRT1 enhanced NLRP3 inflammasome activation and subsequent caspase-1 cleavage. On the other hand, NLRP3 siRNA blocked the activation of the NLRP3 inflammasome in HUVECs stimulated with LPS plus ATP. Further study revealed that NLRP3 inflammasome blockade significantly reduced MCP-1 and CRP production in HUVECs. In vivo studies indicated that implantation of the periarterial carotid collar inhibited arterial SIRT1 expression in rabbits. Meanwhile, treatment with a SIRT1 activator decreased the expression levels of MCP-1 and CRP in collared arteries and the interleukin (IL)-1 level in serum. Taken together, these findings indicate that NLRP3 inflammasome activation promoted endothelial inflammation and that SIRT1 inhibits the inflammatory response partly through regulation of the NLRP3 inflammasome in ECs.
PubMed | Xi'an Jiaotong University and Xian No 4 Hospital
Type: Journal Article | Journal: Oncology reports | Year: 2016
The present study aimed to investigate the role of microRNA (miR)-101 in acute lymphoblastic leukemia progression and chemoresistance. Furthermore, a novel target gene of miR-101 was identified. Here, we confirmed that miR-101 was significantly downregulated in the blood samples of patients with T-cell acute lymphoblastic leukemia (T-ALL) compared with the healthy controls, as determined by reverse transcription quantitative polymerase chain reaction (RTqPCR) analysis. The invitro experiments demonstrated that miR-101 significantly repressed the proliferation and invasion, and induced potent apoptosis in Jurkat cells, as determined by CCK-8, flow cytometer and cell invasion assays. Luciferase assay confirmed that Notch1 was a target gene of miR-101, and western blotting showed that miR-101 suppressed the expression of Notch1 at the protein level. Moreover, functional restoration assays revealed that Notch1 mediates the effects of miR-101 on Jurkat cell proliferation, apoptosis and invasion. miR-101 enhanced the sensitivity of Jurkat cells to the chemotherapeutic agent adriamycin. Taken together, our results show for the first time that miR-101 acts as a tumor suppressor in T-cell acute lymphoblastic leukaemia and it could enhance chemotherapeutic sensitivity. Furthermore, Notch1 was identified to be a novel target of miR-101. This study indicates that miR-101 may represent a potential therapeutic target for T-cell acute lymphoblastic leukemia intervention.