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Objective:To investigate the therapeutic effect of the combination of mouse nerve growth factor and edaravone in the treatment of carbon monoxide poisoning and its effect on patients′ cognitive function, lactic acid clearance rate, and related indicators of oxygen free radicals.Methods:A selection of 158 patients with carbon monoxide poisoning in the Huxi Hospital Affilliated Jining Medical College from May 2017 to June 2020 were divided into study group (80 cases) and control group (78 cases) according to the treatment plan. Both groups were given conventional treatment. On this basis, the control group was given edaravone, and the study group was given mouse nerve growth factor combined with edaravone, both of which were treated for 2 weeks. The clinical efficacy of the two groups was compared with those before treatment and 1 week and 2 weeks after treatment. Neurological impairment score (NIHSS), disease severity score (APACHE Ⅱ), cognitive function score (MMSE), serum inflammatory factors [tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), C-reactive protein (CRP)], oxygen free radical related indicators [lipid peroxide (LPO), superoxide dismutase (SOD), gluten Glutathione peroxidase (GSH-PX), malondialdehyde (MDA)] levels, blood lactic acid levels before treatment and lactic acid clearance rates after 12 h, 24 h, 72 h treatment, and statistics of adverse reactions and 30-day mortality.Results:The total effective rate of the study group was higher than that of the control group after 2 weeks of treatment [95.00% (76/80) vs. 78.21% (61/78)] ( P<0.05); NIHSS and APACHEⅡ scores of the study group after 1 week and 2 weeks of treatment Lower than the control group: (6.08 ± 1.15) points vs. (8.94 ± 1.71) points, (4.58 ± 0.74) points vs. (6.32 ± 0.93) points and (6.79 ± 1.03) points vs. (8.02 ± 1.47) points, (5.94 ± 1.47) points vs. (7.25 ± 0.94) points, the MMSE score was higher than that of the control group: (22.09 ± 4.35) points vs. (19.34 ± 5.32) points, (26.05 ± 2.37) points vs. (22.47 ± 4.64) points ( P<0.05) After 1 and 2 weeks of treatment, the serum TNF-α, IL-6, CRP, LPO and MDA levels in the study group were lower than those in the control group: (22.62 ± 4.12) ng/L vs. (29.43 ± 4.68) ng/L and (18.21 ± 2.09) ng/L vs. (24.37 ± 3.16) ng/L, (39.67 ± 4.35) ng/L vs. (52.14 ± 5.48) ng/L and (34.83 ± 3.75) ng/L vs. (41.07 ± 4.09) ng/L, (12.63 ± 1.85) mg/L vs. (17.02 ± 2.47) mg/L and (8.27 ± 1.16) mg/L vs. (11.05 ± 1.62) mg/L, (11.06 ± 1.28) μmol/L vs. (15.97 ± 1.85) μmol/L and (8.24 ± 1.12) μmol/L vs. (12.97 ± 1.40) μmol/L, (7.15 ± 1.16) μmol/L vs. (9.02 ± 1.47) μmol/L and (6.12 ± 0.96) μmol/L vs. (7.84 ± 1.25) μmol/L, the levels of SOD and GSH-PX were higher than those in the control group ( P<0.05); the lactate clearance rate in the study group was higher than that in the control group after 12, 24 and 72 h of treatment: (18.49 ± 3.63)% vs. (14.62 ± 2.95)%, (23.19 ± 4.20)% vs. (17.42 ± 3.57)%, (29.86 ± 6.37)% vs. (25.38 ± 5.21)% ( P<0.05); the incidence of adverse reactions in the study group during treatment Compared with the control group, there was no significant difference ( P>0.05); there was no significant difference in the 30-day mortality between the study group and the control group ( P>0.05). Conclusions:The combination of mouse nerve growth factor and edaravone in the treatment of carbon monoxide poisoning can reduce the severity of disease and neurological deficits, improve cognitive function and lactate clearance rate, reduce inflammation and oxidative stress, improve efficacy, and have good safety.
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Objective To investigate the protective effects of the total bakkenolides from P.tricholobus on improving hypoxia tolerance in mice. Methods Mice normobaric pressure hypoxia model and oxygen glucose deprivation model in PC12 cells were established, and the effects of PTB on survival time, serum lactate dehydrogenase (LDH) activity and malondialdehyde (MDA) content, brain and heart superoxide dismutase (SOD) and reduced glutathione (GSH) activities, brain tissue pathological changes and cell survival were observed. Results The total bakkenolides from P.tricholobus had prolonged the survival time of mice in confined spaces, increased the activity of SOD and GSH, reduced the production of lipid peroxidation, decreased the degree of anaerobic glycolysis, protected the structure and function of neural cells, and improved the survival rate of OGD-treated cells. Conclusion The total bakkenolides from P.tricholobus could promote the hypoxia tolerance in mice which might be related to scavenging oxygen free radicals, inhibiting lipid peroxidation reaction and protecting the structures and functions of nerve cells.
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Objective: To explore the effect and mechanism of dihydroartemisinin (DHA) in inducing ferroptosis of tumor cells. Methods: 3,3',5,5'-Tetramethylbenzidine was used to detect the oxygen free radicals (•OH) formed by DHA and FeSO4 in vitro. The cytotoxicity of DHA on HepG2 cells was detected by MTT method (including FeSO4 or deferoxamine pretreated groups). MTT assay was used to investigate the influence of glutathione (GSH) and inhibitor (Fer-1) on cytotoxicity of DHA; DCFH-DA dye was used to investigate intracellular reactive oxygen species induced by DHA (including FeSO4 pretreated groups). C11-BODIPY581/591 and DiO dye were used to examine the influence of DHA (including FeSO4 pretreated groups) on intracellular lipid peroxide formation and cell membrane structure; Glutathione peroxidase assay kit was used to explore the influence of DHA (including FeSO4 pretreated groups) on intracellular activity GPX-4 in HepG2 cells. Results: Fenton-like reaction occurred between DHA and Fe2+, and •OH was produced during the reaction. The half-inhibitory concentration (IC50) of DHA was (39.96 ± 8.78) μmol/L. FeSO4 and deferoxamine could increase or decrease the cytotoxicity of DHA, respectively. After treated with DHA, the intracellular content of reactive oxygen species and lipid peroxide was increased, the cell morphology became larger, and the cell membrane was broken. Compared with the DHA treated group, the FeSO4 pretreated group further increased the intracellular reactive oxygen species and lipid peroxide content, and the cell membrane morphology was completely destroyed. FeSO4 could also enhance the inhibitory effect of DHA on GPX-4 activity. Conclusion: DHA increases intracellular reactive oxygen species through Fenton-like reaction and ultimately induces ferroptosis of tumor cells. In addition, exogenous iron can accelerate the Fenton-like reaction of DHA and accelerate the occurrence and development of ferroptosis of tumor cells.
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RESUMEN Introducción y objetivos: La endometriosis es una de las principales patologías ginecológicas que afecta a mujeres en edad reproductiva. Existen muchas teorías en cuanto a su fisiopatología destacando las alteraciones genéticas y epigenéticas, los desbalances hormonales y otros factores como la inflamación crónica y el estrés oxidativo; pero en realidad, su origen continúa siendo desconocido. Estudios recientes han implicado al estrés oxidativo y la consecuente generación de radicales libres de oxígeno en la fisiopatología de la entidad mediante la generación de inflamación crónica pélvica. El objetivo de este estudio es corroborar que existen vías de estrés oxidativo que se encuentran alteradas en estas pacientes. Métodos: Se realizará un análisis de marcadores de estrés oxidativo en plasma sanguíneo, entre ellos los niveles de proteínas carboniladas y el cociente glutatión oxidado/glutatión reducido (GSSG/GSH), comparando los resultados en pacientes con endometriosis (n=19) versus un grupo control (n=11). Resultados: existe un incremento de las proteínas carboniladas en las pacientes con endometriosis (p < 0,041). No se obtuvieron diferencias estadísticamente significativas en relación al cociente GSSG/GSH o a los niveles de GSH. Conclusión: existe evidencia para relacionar al estrés oxidativo con la fisiopatología de la endometriosis, sin poder determinar a día de hoy que vías de oxidación están implicadas.
ABSTRACT Introduction and objectives: Endometriosis is one of the main gynecological pathologies that affects women of reproductive age. There are many theories regarding its physiopathology highlighting genetic and epigenetic alterations, hormonal imbalances and other factors such as chronic inflammation and oxidative stress; but actually, its origin continues to be unknown. Recent studies have implicated oxidative stress and the consequent generation of oxygen free radicals in the physiopathology of the entity through the generation of chronic pelvic inflammation. The objective of this study is to corroborate that there are oxidative stress pathways that are altered in these patients. Methods: An analysis of oxidative stress biomarkers in blood plasma will be carried out, including carbonylated protein levels and the oxidized/reduced glutathione ratio (GSSG / GSH), comparing the results in patients with endometriosis (n = 19) versus a control group (n = 11). Results: there is an increase of carbonylated proteins in patients with endometriosis (p <0.041). There were no statistically significant differences in relation to the GSSG/GSH ratio or GSH levels. Conclusion: there is evidence to relate oxidative stress to the pathophysiology of endometriosis, without being able to determine to date which oxidation pathways are involved.
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Humans , Female , Oxidative Stress , Endometriosis/diagnosis , Reactive Oxygen Species , Endometriosis/pathology , Glutathione , AntioxidantsABSTRACT
Objective To investigate the effect of sufentanil postconditioning on acute lung in-jury induced by ischemia-reperfusion of uterine in rats.Methods Fourty-five adult female Sprague-Dawley rats were randomly divided into 3 groups(n = 1 5 each):control group (group C),ischemia-reperfusion group (group IR)and sufentanil postconditioning group(group SPC).Group SPC received sufentanil 10 μg/kg via intraperitoneal injection before inducing reperfusion of uterine.Ischemia-reper-fusion of uterine was produced by occlusion of bilateral uterine arteries for 45 min followed by reper-fusion for 2 h in group IR and group SPC.Then the content of tumor necrosis factor-α(TNF-α),mal-odiadehyde (MDA)and superoxide dismutase (SOD)activity were measured in uterus,serum and lung tissue,lung wet to dry weight ratio (W/D),lung permeability index (LPI)were compared. Results Compared with group C,TNF-α,MDA content,W/D and LPI in uterus,serum and lung tissue were significantly increased in group IR and group SPC(P <0.05).TNF-α,MDA content,W/D and LPI in uterus,serum and lung tissue were significantly attenuated in group SPC as compared with group IR (P <0.05 ).Compared with group C,SOD activity in uterus,serum and lung tissue was significantly attenuated in group IR and group SPC (P <0.05).SOD in uterus,serum and lung tissue were significantly increased in group SPC as compared with group IR (P < 0.05 ). Conclusion Sufentanil postconditioning attenuates pulmonary injury caused by ischemia-reperfusion of uterine in rats by inhibiting the inflammatory reaction and suppressing the activation of oxyradical.
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Objective:To investigate the protective effects and possible mechanisms of cortex phellodendri water extract and etha -nol extract on the myocardial injury induced by pituitrin and isoproterenol hydrochloride in rats .Methods:SD rats as the experimental animals were randomly divided into the normal control group , model group , compound Danshen tablets group , phellodendron water ex-tract group and phellodendron ethanol extract group .Pituitrin and isopropyl adrenaline hydrochloride were used to establish the myocar-dial injury model in rats.The serum CK, LDH activity, myocardial tissue SOD activity and MDA content were detected and compared . Results:Compared with those in the normal control group , the serum LDH activity , CK activity and MDA content were significantly in-creased , and the SOD activity in cardiac muscle and myocardial tissue was significantly decreased in the pituitrin -established myocardi-al injury model group (P<0.01).In the isopropyl adrenaline hydrochloride-established myocardial injury model group , the MDA con-tent in myocardial tissue was obviously increased , and the SOD activity in myocardial tissue was decreased obviously (P<0.01).The serum LDH activity, CK activity and MDA content were significantly decreased , and the SOD activity in cardiac muscle and myocardial tissue was increased significantly in all drug-taken groups when compared with those in the pituitrin-established myocardial injury model group, and the differences were statistically significant (P<0.05 or P<0.01).The MDA content in myocardial tissue was significant-ly reduced , and the SOD activity was increased significantly in all drug-taken groups when compared with those in the isopropyl adrena-line hydrochloride-established myocardial injury model group , and the differences were statistically significant (P<0.05 or P<0.01). Conclusion:Cortex phellodendri extract has certain protective effect on myocardial injury induced by pituitrin and isopropyl adrenaline hydrochloride in rats .
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Objective To investigate the effect of propofol on rat′s limb ischemia reperfusion injury .Methods Sixty healthy SD rats were randomly divided into sham operate group ,ischemia-reperfusion group and propofol group (n= 20) ,each group was divided into 4 subgroups according to the different reperfusion time .To copy the right lower limb ischemia reperfusion model ,5 min before reperfusion ,use propofol injection (50 mg/kg ,intraperitoneal inject) ,various subjects in the corresponding time points (3 ,6 , 9 ,12 h) were sacrificed .TNF-α ,NF-κB of blood and MDA ,SOD of Skeletal muscle were measured ,calculate muscle wet dry weight ratio .Results Compared with ischemia reperfusion group ,propofol could significantly reduce expression of TNF-alpha ,NF-κB lev-els in serum (P< 0 .05) ,inhibit the increase of the MDA level and decrease of the SOD level in muscle (P< 0 .05) ,also reduce the extent of skeletal muscle cell edema(P< 0 .05) .Conclusion Propofol can attenuate limb ischemia reperfusion injury by inhibiting inflammation response and reducing the oxygen free radicals′ damage .
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Objective To observe the effect of salvia miltiorrhiza injection on antioxygen free radicals and its efficacy on viral myocarditis. Methods 72 cases of patients with viral myocarditis were randomly divided into two groups.The traditional group with energy mixture,1.6-diphosphate fructose improving myocardial nutrition,bed rest,intensive use of glucocorticoid,selected the appropriate treatment for arrhythmia;salvia miltiorrhiza group in the control group treatment combined with salvia miltiorrhiza injection of 5 ~15 mL each time,dissolved in 5%glucose intravenous drip,once a day,2 weeks as a course of treatment.To observe two groups of manifestation,the change of myocardial enzyme spectrum and the comparative efficacy before and after the treatment.Through the detection of the treatment group and the control group of serum superoxide dismutase (SOD ), malondialdehyde (MDA)and other indicators to understand the antioxidant effect of salvia miltiorrhiza injection.36 healthy children were taken as control group,detected cardiac troponin (cTnT),high sensitive C reactive protein (hs-CRP),creatine kinase isoenzyme MB (CK-MB)and SOD in three groups,their correlations were evaluated as well.Results Compared with healthy children,the activity of SOD in salvia miltiorrhiza group was statistically significant (P<0.01).The activity of SOD increased significantly (P<0.01).SOD was negatively correlated with cTnT,hs-CRP and CK-MB levels (P<0.05 ).The curative effect of salvia miltiorrhiza group were significantly higher than that of the control group.CTnT,hs-CRP and CK-MB levels decreased significantly after treatment (P<0.05 ),which in salvia miltiorrhiza group decreased significantly than that of the control group.SOD activity increased value was higher than the traditional group (P<0.01 );the decrease in MDA was obvious than that of the traditional group (P<0.05 ).Conclusion Oxygen free radicals are involved in the pathogenesis of viral myocarditis;the efficacy of salvia miltiorrhiza injection in the treatment of viral myocarditis is proved of curative effect;antioxidant effect may be an important mechanism of salvia miltirrhiza injection in the treatment of viral myocarditis.
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Aim To investigate the effects of echina-coside ( ECH ) on the learning and memory capacities and brain level of oxygen free radicals of rats with de-mentia induced by amyloid β-peptide. Methods Six-ty Sprague Dawley rats, weighing (300±10) g, were randomly divided with 10 rats pergroup into 6 groups:sham operated group, model, ECH high dose (40 mg ·kg-1·d-1), ECH middle dose (20 mg· kg-1· d-1), ECH low dose (10 mg·kg-1·d-1) and Hup A (Huperzine A, 0. 02 mg·kg-1·d-1) group. Mor-ris maze tests were conducted for evaluating the learn-ing and memory ability. Content of malondialdehyde (MDA), nitric oxide (NO) and activities of superox-ide dismutase ( SOD) and NO synthase ( NOS) in the hippocampus and cortex were detected. ResultsAβ25-35 induced significant learning and memory im-pairment in the rats. Compared with the rats in model group, those treated with ECH at different doses all manifested alleviation of learning and memory impair-ment ( P<0 . 01 , P<0 . 05 ) . Cotents of MDA of ECH treatment group were obviously decreased, while SOD activities were obviously increased, and significantly reduced the release of NO and NOS in the hippocam-pus and cortex brain tissue ( P <0 . 01 , P <0.05 ) . Conclusion ECH can enhance the learning and mem-ory ability in rats with AD, which is presumably relat-ed to accelerating the cleaning of oxygen free radicals and reducing oxidative stress in brain of AD rats.
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Aim To investigate the effects of ghrelin on alcohol-induced liver injury. Methods The alcoholic liver injury mouse model was induced by chronic etha-nol feeding ( 4-week ad libitum oral feeding with the ethanol liquid diet) plus a single binge ethanol (5 g· kg-1 ) feeding. The level of alanine aminotransferase (ALT), aspartate aminotransferase (AST) in serum, malondiadehyde ( MDA ) content, superoxide dis-mutase (SOD) and glutathione peroxidase (GSH-Px) activities in liver homogenate were assayed by spectro-photometer. Hepatic pathological examination was ob-served by HE staining. The mRNA expression of proin-flammatory cytokines including TNF-α, IL-1β, IFN-γ, IL-6 and MCP-1 in the liver was measured by real-time PCR method. Results This chronic-plus-single-binge high dose ethanol feeding synergistically induced liver injury, inflammation and fatty liver change. Treatment with Ghrelin ( 5 , 10 , 20 μg · kg-1 ) significantly de-creased the enhanced level of transaminase ( ALT, AST) in serum, improved the pathologic change in liv-er, and reduced the infiltration of inflammatory cells induced by alcohol administration. Ghrelin also de-creased MDA content and increased the reduced SOD and GSH-Px level in liver homogenate. Furthermore, ghrelin decreased inflammatory cytokines mRNA ex-pression including TNF-α, IL-1β, IFN-γ, IL-6 and MCP-1 in the liver. Conclusion Ghrelin has protec-tive effects against alcoholic liver injury in mice via in-hibiting inflammation and suppressing oxidative stress.
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Objective To investigate the effects of preconditioning with ω-3 polyunsaturated fatty acid (ω-3 PUFA) on the second liver injury in rats with traumatic brain injury and hemorrhagic shock (TBIS) and explore the underlying mechanism.Methods Total of 36 male Wistar rats were assigned randomly (random number) into 3 groups (n =12 in each):sham operation group (C),TBIS model group and PUFA pretreatment group.The arterial blood samples were taken for determination of serum levels of ALT,AST and TNF-α.The liver were removed for determination of levels of superoxide dismutase (SOD),malondialdehyde (MDA) and glutathione (GSH),and microscopic examination.Results Compared with group C,the serum levels of ALT,AST and TNF-α and the liver levels of MDA were significantly higher (P ＜0.01),but the liver levels of SOD and GSH in group TBIS and group PUFA were significantly lower (P ＜0.01).The serum levels of ALT,AST and TNF-α and the liver levels of MDA were significantly lower (P ＜ 0.01 or P ＜ 0.05),but the levels of SOD and GSH in liver tissues were significantly higher (P ＜ 0.01or P ＜ 0.05) in group PUFA than those in group TBIS.Histological examination revealed the injury of liver in TBIS group,and the rats in PUFA treated group showed alleviated severity of liver injury.Conclusions The supplementation of ω-3 PUFA can ameliorate acute liver injury in rats with TBIS,which may contribute to inhibition of oxygen free radicals and inflammatory cytokines expression.
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ObjectiveTo observe the subcutaneous and intraperitoneal insulin injection's effect of the level of oxygen free radicals of type 2 diabetes model.MethodsC57BL/6J mice were chosen as normal control group (C group,n=9).KK mice were randomly divided into intraperitoneal injection of insulin group (i.p.group,n=9),the subcutaneous insulin group (s.c.group,n=9) and untreated group (U group,n =9).The i.p.group and the s.c.groups were given certain amount of insulin (insulin injecta and protamine insulin injecta by volume ratio of 2:1 mixture)for one month,maintained the GLU at normal levels (6±1.5) mmol/L.SOD,GSH-PX activity and MDA content of serum,liver,kidney and heart in each group were detected.Results The liver,kidney,heart and serum's SOD and GSH-PX activity significantly reduced and MDA content significantly increased in the U group.Both kinds of delivery methods could increase serum SOD and GSH-PX activity and reduce the content of MDA to the normal control group level,but the intraperitoneal injection had stronger effect.Two kinds of delivery methods could both reduce the MDA content of liver,and had almost the same effect; but the subcutaneous injection group had better effect on increasing the liver's SOD activity,and the intraperitoneal injection had better effect on increasing liver's GSH-PX activity.Intraperitoneal injection had better effect on reducing kidney' s MDA content and increased SOD activity.Two kinds of delivery methods had the same effect on reducing the heart's MDA content.Conclusion The two delivery methods can both make the MDA levels of KK mice in serum,heart,liver and kidney fall to as normal as that of control group,but the two delivery methods have different ways of improving the antioxidant capacity in different organs.Intraperitoneal injection can reduce MDA content in serum and kidney better.
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Aim To investigate the potential role of desipramine(DP) on lipoplysaccharide（LPS）-induced acute lung injury(ALI)and the mechanism of its action.Methods Kunming mice were divided into four groups randomly:NS group(NS),DP control group(DP),LPS group(LPS)and DP treatment group(DP+LPS).The model of ALI in mice was induced by lipoplysaccharidel(LPS,10 mg·kg~(-1),ip).Six hours after LPS challenged,the lung samples were taken for determination of lung wet-to-dry weight ratio(W/D),myeloperoxidase(MPO)activity,and malondialdehyde(MDA)content.The bronchoalveolar lavage fluid(BALF)samples were analyzed for total protein concentrateion and white blood cell(WBC)count.The levels of tumor necrosis factor-α(TNF-α)in lung were measured by ELISA.Results LPS could significantly increase the total protein concentration and WBC number in BALF.The lung W/D ration,MPO activity,MDA content and the levels of TNF-α in lungs all increased after ip injection of LPS.Pretreatment with DP decreased all the changes induced by the LPS.Conclusion Pretreatment with DP protects lung from LPS-induced lung injury in mice,which is,at least in part,through inhibiting the level of TNF-α and decreasing the sequestration of neutrophils and lipid peroxidation.
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Objective To study the preventive effects of erythropoietin (EPO) on acute tubular necrosis of kidney in rats. Method The rat models of acute renal tubular necrosis were established with injecting glycerol in dose of 10 mL/kg. Thirty Wistar rats were randomly (random number) divided into control group, model group and EPO treatment group. EPO was administered intravenously into rats of treatment group in a dose of 1000IU/kg. Levels of blood urea nitrogen (BUN) and serum creatinine (Scr), urine osmolality, urine N-acetyl-D-glucosaminidase (NAG), urine β2-microglobulin (β2-MG), tissue MDA and SOD of rats in the three groups were assayed after the experiment. Renal histological examination was also performed. Results Compared with model group, the levels of BUN and Scr, urine osmolality, NAG,β2-MG and tissue MDA in EPO treament group were significantly lower, but urine osmolality and tissue SOD of rats remarkably increased in comparison with model group. EPO also lessened the histological changes in treatment group. Conclusions EPO has some protective effects on acute renal tubular necrosis in rats, which is probably through preventing oxygen free radical damage and elevating endogenous antioxidation potential.
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Objective To investigate the effects of hyperbaric oxygen (HBO) therapy following spinal cord injury (SCI) and its mechanisms. Methods Thirty Sprague-Dawley rats were randomly divided into two groups after inducing SCI models using a modified version of Allen's method. The HBO group received HBO treatment 2 h after the procedure and were then treated 100 min every day for 5 consecutive days. All the rats were evaluated 1 h before the operation, and 1 h, 10 d and 20 d afterward using BBB scores and inclined plane experiments. Superoxide dismutase (SOD) and malondialdehyde (MDA) levels were measured. At twenty days, all the rats were sacrificed and their spinal cords were examined pathologically using HE staining. Results Average BBB scores and climbing ability in the HBO group were better than in the control group at the 10th and 20th day after the operation. Compared to the control group, SOD increased significantly and MDA decreased significantly in the HBO group at the 2nd and 5th day after the operation. There was less cystic degeneration of the spinal cord in the HBO group. Conclusions HBO demonstrated a positive effect after SCI. Oxygen free radicals might be one of the mechanisms for the better recovery.
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[Objective] To observe the effect of Leweiyin of traditional Chinese compounds prescription on gastrointestinal hormones and oxygen free radicals in IBS rabbits of spleen deficiency,and to explore the possible mechanism for the treatment of IBS with spleen deficiency.[Methods] 36 two-month-old rabbits with white feather and black eyes(WHBE rabbit),half male and half female,were randomly divided into 6 groups:normal group,model group,Xiangsha Liujun pill group,Lizhu Changle group,low-dose Leweiyin-treated group,high-dose Leweiyin-treated group.Except the normal group,others were made into IBS model of spleen deficiency which was induced by damp heat stress and gavage with Fanxieye as well as method of either hunger or gorge.The drug groups were administered preventively from the medium-term of the model reproduction to the end of modeling.The rabbits of each group were observed.NO,NOS,MDA,SOD in serum and SP in colonic membrane were detected.[Results] NO,NOS,MDA in serum and SP in colonic membrane significantly more increased than the normal group(P
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Objective To explore the role of oxygen free radicals in the proliferation of ECV304 induced by AngⅡ.Methods The lines of human umbilical vein endothelial cell(ECV304)cultured in vivo were divided into three groups which were treated by AngⅡ,AngⅡ+N-acetyl-L-cysteine(NAC),and normal culture medium.First we observed the proliferous effect of ECV304 induced by AngⅡat different concentration with improved MTT and microscope.Then the contents of oxygen free radicals(?OH)in three groups were detected by spectrophotometer.Results ECV304 incubated with AngⅡ(0.03125～1?mol/L)for 12 hours increased the proliferation rate(P 0.05 vs.control group).Conclusions ECV304 induced by AngⅡcan produce oxygen free radicals(?OH),and the contents of oxygen free radicals(?OH) increase with the prolongation of time and the enlargement of dose;Antioxidant NAC can inhibit the proliferation of ECV304 induced by AngⅡ,this effect may be related with reducing the content of oxygen free radicals(?OH);oxygen free radicals(?OH)may be one of the major mocleculars which play an important role in the signal transduction of ECV304 proliferation.
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Objective To investigate the effect of oxygen free radicals on the myocardial injury in acute MODS.Methods Thirty-six SD rats were randomly divided into two groups.The rats of experimental group were peritoneally injected with the suspension of zymosan-parogen.The rats of control group were injected with steriled saline at the same volume.The dynamtic change of LPO,SOD,myocardial enzyme in plasma and MDA,SOD in myocardial tissue at different time point were detected.The pathologic change of myocardial tissue by HE staining was observed.Results Compared with the control group,the LPO,MDA,CKMB,LDH,GOT in plasma and myocardial tissue increased at 6 hours (P
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Epilepsy is a neurological disorder from many molecular and biochemical responses. In the underlying mechanism, free radicals play an important role in seizure initiation and seizure-induced brain damage. Excessive production of oxygen free radicals and other radical species have been implicated in the development of seizures under pathological conditions and linked to seizure-induced neurodegeneration.
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Brain , Epilepsy , Free Radicals , Nervous System Diseases , Oxygen , SeizuresABSTRACT
AIM: To evaluate the protection of Mn~(2+) on injury of human kidney tubular epithelial cell line induced by gentamicin, and investigate its principals. METHODS: Gentamicin was used to injury human kidney tubular epithelial cell line (HK-2) to produce model of kidney injury. MTT method was used to measure effect of Mn~(2+) on proliferation of cells after they were injured by gentamicin. The spectrophotometry method was used to observe the change of LDH,NAG and SOD effected by Mn~(2+). Ultrastructure was examined by electron microscopy. RESULTS: Although HK-2 cells were injured, Mn~(2+) promoted cells proliferation, decreased LDH activity and NAG content, increased SOD activity, and alleviated dilation of the mitochondria and crushing of lysosomes. CONCLUSION: Mn~(2+) can protect human kidney tubular epithelial cell line from injury induced by gentamicin. It may be in relation to inhibiting the oxidative injury, lightening dilation of the mitochondria, protecting the integrity of lysosomes and decrease the leakage of enzyme.