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@#Abstract: - Well characteristic biomarkers are helpful for understanding the disease condition of patients with occupational pneumoconiosisand predictthediseaseevolution.Currently,related biomarkersarewidelystudied and theyinclude:epithelial cell injury related biomarkers such as salivary glycochain antigen, Clara cell protein and surfactant protein; inflammatory - - response related biomarkers such as interleukin, tumor necrosis factor α, chemokine, high mobility group protein 1 and - - L selectin; oxidative stress related biomarkers such as superoxide dismutase, glutathione, malondialdehyde, heme oxygenase 1 and lactate dehydrogenase; pulmonary fibrosis related biomarkers such as matrix metalloproteinases and transforming growth - - - - - factor β; non coding RNA such as miR 19a, miR 29 and miR 146a, et al. These biomarkers are helpful to understand the pathogenesisofoccupationalpneumoconiosisandguidethediagnosis,treatmentandprognosis.However,moreresearchneedsto-bedoneontherepeatabilitytestofbiomarkers,combinedapplicationandtheminingofnoncodingRNAastargetsfordisease diagnosisandtreatment.
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Objective To investigate the effects and mechanism of dexmedetomidine hydrochloride preconditioning against glutamate-induced neurotoxicity.Methods The model of glutamate-induced neurotoxicity was established by the injection of glutamate into lateral cerebral ventricle.Thirty-six SD rats were randomly divided into control group (C group),glutamate-induced neurotoxicity group (G group),Dex1 group and Dex2 group.Dex1 group and Dex2 group received intraperitoneal injection of dexmedetomidine respectively at a dose of 50 μg/kg or 100 μg/kg before glutamate application.Two hours later,the rats were sacrificed and hippocampus was separated to measure the level of SOD and MDA.The rest of each brain was used to measure the degree of brain edema.Pathological changes were observed under microscope with Nissl's staining.Results In contrast to G group,brain edema and MDA concentration in Dex1 group and Dex2 group were significant lower,while SOD concentrations were significantly increased and the pathological change in Dex1 group and Dex2 group were relieved obviously compared to glutamate-induced neurotoxicity group.Conclusion Dexmedetomidine preconditioning can significantly attenuate glutamate-induced neurotoxicity,which is properly related to the inhibition of oxidative-stress reaction.
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Objective To investigate the significance of variation of concentrations of serum IL-1,IL-6, TNF-α and cyclooxygenase-2 in patients with post-traumatic stress disorder (PTSD). Methods Thirty-two PTSD patients were chosen as the observation group and another 26 normal patients were taken as the control group. The concentrations of serum IL-1,IL-6,TNF-α and COX-2 in patients of both groups were detected by Enzyme-linked immunosorbent assay (ELISA) and Western blot and were compared in these 2 groups. Results The concentrations of serum IL-1 , IL-6 and TNF-α were significantly higher in the observation group than those in the control group (P < 0.01);and the level of COX-2 in the observation group was significantly higher than that of the control group(P < 0.01). Conclusions Abnormal immune states are awared in PTSD patients and the IL-1,IL-6,TNF-α and COX-2 might play an important role in the pathogenesis of PTSD.
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[ABSTRACT]AIM:Toexploretheeffectsofchrysinoninsulinresistance(IRe)inamousemodel.METHODS:Male C57 mice were randomly divided into control group , IRe group, low-dose chrysin group ( IRe+chrysin-low) and high-dose chrysin group (IRe+chrysin-high).After 24 weeks, the body weight, liver index and fat mass in all mice were detected.The blood glucose , insulin level and HOMA-IR were measured to determine the changes of the insulin resistance in the animals.The oxidative stress (SOD, GSH-Px and MDA) was also measured.The mRNA expression of insulin sig-naling pathway molecules (IR, IRS1, IRS2, Glut2 and Glut4) and inflammatory factors (TNF-α, IL-1β, IL-6 and NF-κB) was analyzed by real-time PCR.The protein levels of IRS1 and p65, and their phosphorylation were detected by West-ern blot.RESULTS:After 24-week intervention , the indicators in IRe group were higher than those in control group , in-cluding body fat deposition, serum glucose, serum insulin, HOMA-IR and liver oxidative stress (P<0.01), indicating that the model of insulin resistance was successfully established .Low dose and high dose of chrysin decreased the body weight, serum glucose, serum insulin and HOMA-IR in the IRe mice (P<0.05).The liver oxidative stress was also re-duced in both groups (P<0.05).However, no statistical difference of the indexes between IRe +chrysin-low group and IRe+chrysin-high group was observed.Chrysin upregulated the mRNA expression of IR , IRS1, IRS2, Glut2 and Glut4 (P<0.05), and down-regulated the mRNA expression of various inflammatory factors .The inhibitory effect of chrysin on the mRNA expression of NF-κB was observed (P<0.05), especially in high dose group (P<0.05).It was confirmed that the effect of chrysin on liver IRe was related with the increase in the p-IRS1 levels and decrease in the p-p65 levels by Western blot .CONCLUSION:Chrysin inhibits obesity , hyperglycemia and hyperinsulinemia , and relieves insulin resist-ance and oxidative stress , which might be closely related to the regulation of insulin signaling pathway and the inhibition of inflammatory factor expression .
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Objective To investigate the protective effect of hydrogen-rich saline on systemic oxidative stress in rats with severe traumatic brain injury(STBI) .Methods Male Wistar rats(n=60) were divided into three groups randomly :sham group ,STBI+normal saline group ,STBI+ hydrogen-rich saline group .STBI model was induced by controlled cortical impact injury .Hydrogen-rich saline were intraperitoneally administered at 5 min after STBI operation .Plasma malondialdehyde (MDA ) ,Superoxide Dis-mutase(SOD) activity and glutathione peroxidase(GSH-PX) activity were measured before TBI operation ,12 ,24 h and 48 h after TBI operation .Results The level of MDA in STBI group plasma was significantly elevated from 24 h to 48 h after STBI operation (P< 0 .05) .Hydrogen-rich saline treatment significantly attenuated the increase of MDA level in STBI operation animals (P<0 .05) .The activities of SOD and GSH-PX were slightly elevated at 6 h after TBI operation ,but decreased significantly from 24 h to 48 h after STBI operation(P<0 .05) .Hydrogen-rich saline treatment significantly increased the activities of SOD and GSH-PX after STBI operation(P<0 .05) .Conclusion Hydrogen-rich saline could exert a protective effect against STBI via reducing oxidative stress .Molecular hydrogen might be a more effective therapeutic strategy for TBI patients .
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New progress in the area of nanoparticle research are the studies on interactions between nanoparticles (NPs) and biological molecules in body fluid,cellular microenvironment,intracellular components or secreted cellular proteins such as cytokines,growth factors and enzymes and the use of engineered NPs to target various signal transduction pathways in cancer therapy.NPs-induced toxicological mechanism has become one of the most studied topics.Oxidative stress result is not sufficient to explain all the biological effects.This article reviews the latest research progress in nanotoxicology from the perspective of cellular mechanisms,including the interactions between NPs and the cell membrane receptor,cell oxidative stress result,cell apoptosis induction and the effects of NPs on cell cycle.
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This research attempts to examine the effects of ascorbic and folic acid intervention on the haematology, antioxidants molecules and enzymes of mice exposed to malaria infection. The study involves three groups of control (non-parasitized-nontreated), parasitized-nontreated (PnT) and parasitized ascorbic and folic acid treated (P+as+faT). Intervention with ascorbic and folic acids commenced for three days after parasitemia had been established in mice. Results from this study showed that ascorbic and folic acid intervention in malaria condition reduced (P<0.05) total protein, erythrocyte fragility (EF), increased (P<0.05) packed cell volume (PCV) in comparison with PnT and control mice groups. Lipid peroxidation product in serum, Superoxide dismutase (SOD) activity and Catalase (CAT) activity and reduced glutathione (GSH) reduced in parasitized mice administered with ascorbic and folic acid doses, as against those of control, whereas SOD activity in Control and CAT activity in PnT observed to increase and decrease, respectively. The extent of lipid peroxidation in kidney was effectively reduced by ascorbic and folic acid compared to PnT. In liver SOD activity, CAT activity, glucose-6-phosphate dehydrogenase (G6PD) activity significantly (P<0.05) reduced in P+as+faT as against PnT and control groups. From these observations therefore, we draw the conclusion that ascorbic and folic acids combination in malaria infection may reduce lipid peroxidation and stimulate cellular pathways that enhance the production of high concentrations of hydrogen peroxide.
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<b>Objective</b>: <i>Lentinus edodes</i> (Shiitake) is a very popular mushroom in Asian cuisine. The water-soluble extract from culture medium of <i>Lentinus edodes</i> mycelia (LEM), which is commercially available as a nutritional supplement, is prepared by hot-water treatment from a solid medium composed of bagasse and defatted-rice bran overgrown for about 4 months with its mycelia. LEM was previously reported to have antioxidant activity and to suppress various oxidative damages. In this study, the neuroprotective effects of 2-week intake of LEM on cerebral ischemic damage induced by hypoxia/ischemia (H/I) followed by reoxygenation in mice were examined.<br> <b>Method</b>: Male C57BL/6J mice were divided into three groups, fed for two weeks with the control laboratory powder chow, 0.5% LEM-contained chow, or 1% LEM-contained chow, respectively. Cerebral ischemic damage was induced in the mice by H/I (i.e., unilateral ligation of the carotid artery and exposure of 8%O<sub>2</sub> for 30 min). Twenty-four hours after H/I, total plasma oxidative stress, neurological deficits, cerebral infarction volume were evaluated in each group. Furthermore, the number of apoptotic cells in ischemic penumbra, the hippocampal CA1 and CA2, and the somatosensory area of the cortex, were analyzed by TUNEL staining and cleaved caspase-3 immunostaining.<br> <b>Results</b>: The infarct area assessed 24-h after H/I was extended to the corpus striatum and cortex in the control mice. Treatment of LEM dose dependently improved plasma oxidative stress, neurological deficits, and cerebral infarction volume. Moreover, LEM decreased the levels of dihydroethidium activity as an index of super oxide production and the number of apoptotic cells in ischemic penumbra.<br> <b>Conclusion</b>: These results show that chronic intake of LEM relieves the hypoxia-induced cerebral ischemic injury, which may be attributed to the antioxidant effects of LEM.<br>
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Objective To study the effect of fosinopril on the expression of NADPH oxidase subunit p22phox mRNA and the extracellular matrix (ECM) accumulation in the kidneys of rats with diabetes mellitus . Methods Diabetic rats induced by streptozotocin were randomly divided into control group(DM group) and fosinopril group (fosinopril 10 mg'kg-1·d-1) (DM+Fosin group) and treated for 12 weeks . Expression of p22phox mRNA of NADPH oxidase in kidneys was measured by RT-PCR . The expression of fibroneetin was studied by immunohistochemistry and matrix metalloproteinases 9 activity was detected by Zymography . Meanwhile, the kidney hypertrophy index, serum creatinine level and 24-hour urinary protein excretion were evaluated . Results The expression level of p22phox mRNA in the kidneys of DM+Fosin group rats was decreased by 45% than that of DM group at week 4 (P＜0 .05) . At week 8 fosinopril significantly decreased the expression of glomerular and tubulointerstitial fibronectin by 52,5% and 42 .9% respectively (P＜0 .05), while increased MMP-9 activity by 29 .6% (P＜0 .05) compared with DM group . Fosinopril significantly decreased 24-hour urinary protein excretion of diabetic rats from week 8 . Serum creatinine level, 24-hour urinary protein excretion and kidney hypertrophy index were significantly decreased by 35 .9%, 50 .2% and 17 .2% in rats of DM+Fosin group than those of DM group at week 12 (P＜0 .05) . Fosinopril did not affect blood sugar significantly . Conclusion Fosinopril has beneficial effect on diabetic nephropathy partly through inhibiting the expression of NADPH oxidase p22 phox mRNA .
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<i>Objective</i>: In this study, the neuroprotective effects of a water-soluble extract from culture medium of <i>Ganoderma lucidum</i> mycelia (WER) on oxidative stress-induced injury were examined using H<sub>2</sub>O<sub>2</sub>-treated PC12 cells. Additionally, we investigated both the acute and chronic effects of WER on brain necrosis and apoptosis induced by hypoxia/ischemia (H/I) followed by reoxygenation in mice.<br> <i>Methods</i>: Viability and apoptosis index of H<sub>2</sub>O<sub>2</sub>-treated PC12 cells were determined by 3,4,5-dimethylthiazol-2-yl (MTT) assay and TUNEL staining, respectively. H/I in mice was induced by unilateral ligation of carotid artery and exposure of 8%O<sub>2</sub> for 30 min. Twenty-four hours after H/I, neurological deficits, cerebral infarction volume, and apoptosis level were evaluated.<br> <i>Results</i>: WER–pretreated PC12 cells showed an increased viability evaluated by MTT assay compared to untreated cells. TUNEL staining indicated that WER induced a concentration-dependent decrease of the number of apoptotic cells. In the mouse model of H/I, acute (pre-H/I) treatment of WER (1 g/kg, p.o.) did not affect neurological deficits, total plasma oxidative stress, cerebral lipid peroxidation, and infarction volume assessed 24-h after reoxygenation. However, chronic treatment of WER (1 g/kg, p.o., for 7 days) significantly improved these parameters compared with distilled water-treated mice. Moreover, chronic treatment of WER decreased the levels of apoptosis in two brain areas, the sensori-motor cortex and the CA1 of the hippocampus, analyzed by TUNEL and cleaved caspase-3 immunostaining.<br> <i>Conclusion</i>: These results show that daily intake of WER relieves the cerebral ischemic injury, which may be attributed to decrease of oxidative stress.<br>
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Aim To study antidiabetic effect and mechanism of Mogroside extracts(MGC) on hyperglycemic mice induced by Alloxan.Methods Alloxan-induced diabetic mice were fed with MGC at dose of 50,100?300,500 mg?kg~(-1) bw respectively for 30 d.The blood glucose levels,the blood lipid levels and antioxidation levels were assayed after the last fedding.Results ①MGC at dose of 100?300?500 mg?kg~(-1) bw significantly lowered the fasting blood glucose and the hypoglycemic effect of MGC at dose of 100 mg?kg~(-1) bw was the best ②MGC decreased the content of TC,TG and enhanced the content of HDL-C of alloxan-induced diabetic mice,so it could restore the blood lipid levels of diabetic mice(P0.01).Conclusion Mogroside extracts(MGC) have obvious glucose-lowering effect on hyperglycemic mice,its mechanism may be related with improving antioxidation level and restoring the blood lipid levels of hyperglycemic mice.
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Objective:To study the effects of Probucol and Fosinopril on liver histological changes in type 2 diabetes mellitus. Methods: Male Wistar rats,weighing 140～160 g,were fed with chowdiet for one week,and then randomly divided into two groups:the control group (C,twelve rats)was fed with chowdiet,while another group(thirty-six rats)was fed with high-fat diet. The rats in high-fat diet group were successfully established as type 2 diabetes model four weeks later (fasting serum glucose≥7.8 mmol/l)through streptozocin (STZ)(35 mg/kg)intraperitoneal injecting,then randomly divided into three groups (twelve rats each group):Rats in Probucol group were fed with high-fat diet and Probuco(l500 mg(/kg?d),lavage);Rats in Fosinopril group were fed with high-fat diet and Fosinopri(l5.0 mg(/kg?d), lavage);Rats in simple high-fat diet group were fed with high-fat diet and water(2 ml(/one?d),lavage). Six weeks later,ratio of liver to body weight,serum ALT,AST,TG,TCHO,HDL,MDA and SOD activity,histological scoring for Nonalcoholic fatty liver disease(NAFLD) were measured respectively. Results:TCHO and ALT were significantly reduced by Probucol treatment compared with HD group (P