Intervention of Astragalus membranaceus on radioactive lung injuries and influence on TNF-α and ET expression

Objective To observe the lung protection of Astragalus membranaceus against radiotherapy to intermediate-stage and terminal thoracic neoplasm, and its influence on TNF-α and ET expression.Methods The patients with intermediate-stage and terminal thoracic neoplasm under radiotherapy were divided into a treatment group and a control group.Patients in the treatment group took 10 ml of Asragalus membranaceus twice a day.for consecutive 6 months from the beginning of radio therapy.TNF-α and ET in the plasma were measured before and after the radiotherapy.The clinical symptom,iconographic changes and lung diffusion were observed from the 15th day of radiotherapy.Results The TNF-α and ET in plasma afterthe radiotherapy were(2.48±0.75)as/ml and(69.32±23.03)pg/ml for the treatment group,and(5.12±1.01)ns/ml and(97.87±37.83)pg/ml for the control group with the statistial difference(x2=7.49,6.57,P<0.001).The decrease of CO diffusion 5 and 10 months after the radiotherapy in the treatment group was statistically different compared with that in the control group(x2=3.98,3.78,P<0.05).There was a statistical difference of the incidence of acute radiation pneumonitis and pulmonary fibrosis between these two groups(P<0.05).Conclusions Astragalus membranaceus could inhibit the excess expression of TNF-α and ET in plasma and reduce the deterioration of diffusion after radiotherapy,so that it can be used for intervention of lung injuries from radiotherapy.     

重组人白细胞介素-11和姜黄素对中子照射致小鼠肠道损伤的治疗作用

Objective To explore the therapeutic effect of recombinant human interleukin(rhIL-11) and curcumin on jejunal damage in mice after neutron irradiation.Methods 140 male BALB/c mice were randomly divided into 4 groups:20 mice in healthy control group,60 mice in mere irradiation group,30 mice in IL-11 treatment group and 30 mice in curcumin treatment group.The mere irradiation group mice were wholly exposed to 3 Gy neutron irradiation.The treatment groups mice were intraperitoneally enterocoelia once a day for 5 d after irradiation.The mortality of the mice were observed.The mice in the control and mere irradiation groups were killed 6 h,1,3,and 6 d post-irradiation,respectively,and the mice of the 2 treatment groups were killed 3 and 6 d post-irradiation,respectively and the samples of jujunum were colleted.HE staining,argyrophilic of nucleaolar organizer regions staining,Feulgen staining,and image analysis were used to observe the pathology and levels of argyrophilic proteins and DNA.Results The mice in the mere irradiation group all died at 5 d post-irradiation,while 2 mice in the IL-11 treatment group and 3 in the curcumin group survived.Large area necrosis and exfoliation were found in the intestinal epithelial mucosa of the mere irradiated group mice since 6 h to 3 d after irradiation.Crypt cell regeneration was seen occasionally found 3 days later and much more 5 days later.Crypt cell regeneration was obviously found in the intestinal epithelial mucosa and lots of new villi were observed 5 d after irradiation in both treatment groups,however,the amounts of crypt cells and new villi of the curcumin treatment group were less than those of the IL-11 treatment group.The contents of AgNOR and DNA in the intestinal epithelial cells 5 days after irradiation of the 2 treatment groups were all significantly higher than those of the mere irradiation group (F = 0.015-0.035,all P ＜ 0.05) but without significant differences between them.Conclusions Jejunal damage in mice could be induced after 3 Gy neutron irradiation.rhIL-11 and curcumin might reduce the damage and promote the regeneration and repair of the intestinal epithelium.     

知母活性成分ZMR对慢性帕金森病模型小鼠多巴胺系统的调节

objective The significant neuropathological features of Parkinson's disease include sharp decrease of striatal dopamine (DA) and downregulation of striatal dopamine transporter (DAT) density in nigrostriatal pathway.The purpose of this research was to investigate the effects of ZMR on the DAT and DA membolism in the brain of a chronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinisen's disease.Metbods C57BL/6 mice were divided into four groups:control mice,model mice,model mice treated with 10 mg/kg of ZMR(ZMR-10)and model mice treated with 26 mg/kg of ZMR(ZMR-26).All mice except control received ten doses of MPTP(15 mg/kg,subcutaneous injection)plus probeneeid(250 ms/kg,intraperitoneal injection)twice a week in five weeks.Mice in groups of ZMR10 and ZMR-26 were administrated 10mg/kg and 26 mg/kg of ZMR by oral gavage once daily for 60 d respectively.Striatal DAT was detected by autoradiography using 125I-2β-carbomethoxy-3B-(4-iodophenyl)-N-(3-fluoropropropyl) nortropane (FP-CIT).Monoamine oxidase B(MAO-B)activity was determined with a commercial kit.DA and its metabolites were determined by high performance liquid chromatography-electrochemical detection(HPLC-ECD).Staffstical analysis was performed with SAS 6.12 software,and the oneway ANOVA,grouped t-test Were used to analyze the data.Results Compared with vehicle treated model mice,ZMR-10 and ZMR-26 increased striatal DAT density from 0.212±0.012 to 0.268±0.019 and 0.281±0.018 respectively(t=2.5314,3.1124,P＜0.05 and＜0.01 respectively),raised striatal DA levels from(3.00±0.25)μg/g to(4.21±0.32)μg/g and(4.58±0.39)μg/g respectively(t=2.9879,3.4163.P＜0.05 and＜0.01 respectively).However.ZMR-10 and ZMR-26 did not affect the MAO-B activity.Conclusion ZMR raises striatal DA levels in chronic MPTP-model mice.which is closely related to the elevation of striatal DAT density but not related to catabolism of DA.     

香兰素衍生物VND3207对小鼠骨髓细胞遗传损伤的防护效应研究

Objective To study the protection of vanillin derivative VND3207 on the cytogenetic damage of mouse bone marrow cell induced by ionizing radiation.Methods BALB/c mice were randomly divided into five groups:normal control group,2 Gy dose irradiation group,and three groups of 2 Gy irradiaiton with VND3207 protection at doses of 10,50 and 100 mg/kg,respectively.VND3207 was given by intragastric administration once a day for five days.Two hours after the last drug administration,the mice were irradiated with 2 Gy γ-rays.The changes of polychromatophilic erythroblasts micronuclei (MN),chromosome aberration (CA) and mitosis index (MI) of mouse bone marrow cells were observed at 24 and 48 h after irradiation.Results Under the protection of VND3207 at the dosages 10,50,100 mg/kg,the yields of poly-chromatophilic erythroblasts MN and CA of bone marrow cells were significantly decreased(t = 2.36-4.26,P ＜ 0.05),and the marrow cells MI remained much higher level compared with the irradiated mice without drug protection (t = 2.58,2.01,P ＜ 0.05).The radiological protection effect was drug dose-dependent,and the administration of VND3207 at the dosage of 100 mg/kg resulted in reduction by 50% and 65% in the yields of MN and CA,respectively.Conclusions VND3207 had a good protection effect of on γ-ray induced cytogentic damage of mouse bone marrow cells.     

放射线联合p53基因及内皮抑素治疗小鼠前列腺癌皮下移植瘤

Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other.     

放射线联合p53基因及内皮抑素治疗小鼠前列腺癌皮下移植瘤

Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other.     

放射线联合p53基因及内皮抑素治疗小鼠前列腺癌皮下移植瘤

Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other.     

富氧吸入对大鼠模拟急性高原肺水肿的防护作用

Objective To investigate the protective effects of oxygen enrichment inhalation on preventing acute high altitude pulmonary edema (HAPE) of rats and compare the effects of various oxygen inhalations. Methods Forty-four male Wistar rats were randomly and averagely divided into control, hypoxia, fulltime oxygen enrichment and nocturnal oxygen enrichment groups. Rats with various inhalations were exposed to simulated 6000 m in hypobaric chamber for 48 h except control group..The wet to dry ratio (W/D), protein concentration of bronchoalveolar lavage fluid (BALF),nitric oxide (NO) content and nitric oxide synthase (NOS) activity in serum and lung homogenate were measured, and lung histological change was determined. Results Comparing with control group, hypoxia group showed significantly increased W/D, BALF protein concentration and decreased NO level and NOS activity (P＜0.01). Interstitial pulmonary edema, haemorrhage and neutrophil infiltration were found in hypoxia group. W/D and BALF protein concentration both in fulltime oxygen enrichment and nocturnal oxygen enrichment groups were decreased compared with those in hypoxia group (P＜0. 05), while the level of NO and the activity of NOS were increased (P＜0. 01).Conclusions Oxygen enrichment inhalation has the protective effects on preventing HAPE by improving NO level and NOS activity. There is no significant different protective effect between fulltime oxygen enrichment and nocturnal oxygen enrichment groups.     

人工富氧环境改善急进高原人员睡眠效果的研究

Objective To study the effects of the artificial oxygen-enriched environment (is called "oxygen-enriched room" in short) on sleep efficiency of the people who participate in the mission on plateau with hurry-up entry,and to investigate the anti-hypoxia effect of oxygen-enriched room to plateau acclimatization. Methods Eighteen subjects were randomly and averagety allocated into plain group,oxygen-enriched group and hypoxia group.Only the later two groups were dispatched to plateau by air.Molecular sieve oxygenerator was used to supply the room with oxygen on 3500 m plateau.The oxygen-enriched group and hypoxia group got into the oxygen-enriched rooms and normal rooms respectively at 22 o' clock and took rest till to 9 o' clock next morning.The changes of heart rate (HR) and the saturation of blood oxygen (SaO2) of three groups were recorded and compared between the states of with and without oxygen enrichment.The subjects were monitored by sleep respiration recording and analysis system. Results ①The SaO2 of the oxygen-enriched group was 92.3%±1.0%,and it was significant higher than the state before oxygen enrichment (82.9%±4.2%) and than that of hypoxia group (79.3%±5.9%,P<0.01),but lower than that of plain group (97.3%±0.8%,P<0.05).②There were less deep sleep and more slight sleep in hypoxia group and oxygen-enriched group than in plain group.The hypopnea and apnea hypopnea index (AHI) of plain group was significant lower than that of hypoxia group and oxygen-enriched group (P<0.05).The AHI of the oxygen-enriched group was 28.1±11.9,and it was significant lower than that of hypoxia group (53.2±23.4)(P<0.05).③The normalized low-frequency (Ln) and the ratio of low-frequency to high-frequency (LF/HF) measured in sleep was respectively 89.3±2.9 and 6.4±1.4 in oxygen-enriched group comparing to 90.2±1.8 and 9.9±1.9 in hypoxia group but without statistical difference.The corresponding Ln and LF/HF of plain group was 85.8±2.9 and 6.4±1.4 respectively,significantly higher than those of other two groups (P<0.05).Plain group also showed higher normalized high-frequency than others(P<0.05). Conclusions Oxygen-enriched environment can effectively improve the sleep quality but significantly change heart rate variation (HRV) of the people who participate in the mission with hurry-up entry to plateau.Further studies are still needed to reveal the quantitative effectiveness of oxygen-enriched room to plateau acclimatization.     

雌二醇衍生物的结构和抗辐射效价的QSAR分析

34 estradiol derivatives have been tested in mice for their antiradiation activities.The mice were exposed to 750 rads of γ rays.Nine days following irradiation,spleen weights,endogenous spleen colonies,peripheral leucocytes and femoral DNA contents of the treated mice were determined and compared with those of the control which were subjected to irradiation in different doses.     

Is sudden death with vitamin C deficiency caused by lack of carnitine?

We investigated the effect of carnitine supplementation during vitamin C (ASC) deficiency by measuring the levels of ASC and carnitine in plasma and cardiac muscle cells (CMC), and histological analysis with electron microscopy. The levels of carnitine were significantly decreased in ASC-deficient rats in plasma and the heart than those in the control. In carnitine supplemented ASC-deficient rats, a significant increase of carnitine levels were observed in both plasma and heart. The number of lipid droplets significantly increased in the ASC-deficient rats compared to the control rats, but did not increase in carnitine supplemented rats. These results indicate that ASC deficiency causes a generalized mitochondrial abnormality and accumulation of lipid droplets in CMC as observed in carnitine deficiency, and supplementation of carnitine prevented these changes even in the presence of ASC deficiency.     

Muscle soreness and damage parameters after prolonged intermittent shuttle-running following acute vitamin C supplementation

Exercise-induced free-radical production may be partly responsible for muscle soreness and damage following demanding exercise. A number of studies have investigated the effect of antioxidant supplementation although there is a paucity of information regarding vitamin C. Therefore the aim of the present study was to investigate the effect of vitamin C supplementation on exercise-induced muscle soreness and damage. Nine habitually active males consumed a 1 g dose of vitamin C 2 h before exercise, and on another occasion consumed an identical placebo. The exercise comprised a 90 min intermittent shuttle-running test, which was designed to simulate the multiple-sprint sports. Vitamin C supplementation increased plasma concentrations of vitamin C before exercise, and plasma concentrations continued to increase during the shuttle-run to reach a peak of approximately 200 micromol x l(-1) immediately after exercise. However, muscle soreness, and markers of both muscle damage (creatine kinase and aspartate aminotransferase) and lipid peroxidation (malondialdehyde) were elevated to an equal extent after exercise in placebo and supplemented trials. Therefore acute supplementation with vitamin C had no beneficial effects although it is possible that such short-term vitamin C supplementation was ineffective because it occurred at an inappropriate time.     

Vitamin E regulates changes in tissue antioxidants induced by fish oil and acute exercise

PURPOSE: Prooxidant effects of fish oil supplementation could unfavorably affect the cardiovascular benefits of fish oil. We tested the effects of 8 wk vitamin E cosupplementation with fish oil on antioxidant defenses at rest and in response to exhaustive exercise in rats. METHODS: Rats (N = 80) were divided into fish oil, fish oil and vitamin E (FOVE), soy oil, and soy oil and vitamin E (SOVE) supplemented groups. For the vitamin E supplemented rats, corresponding groups (FOVE-Ex and SOVE-Ex) performed an acute bout of exhaustive exercise after the supplementation period. RESULTS: Fish oil supplementation increased the activity of catalase, glutathione peroxidase, and glutathione-S-transferase in the liver and red gastrocnemius (RG) muscle. Fish oil decreased liver total glutathione (TGSH) levels. Vitamin E supplementation decreased antioxidant enzyme activities to levels at or near those in SOVE in a tissue specific pattern. Vitamin E increased TGSH in liver, heart, and RG. Regression analysis showed TGSH to be a negative determinant of protein oxidative damage as measured by protein carbonyl levels in both liver and RG. Catalase activity was associated with liver lipid peroxidation as measured by thiobarbituric acid-reacting substances. The exercise-induced decrease in hepatic TGSH tended to be less in FOVE versus SOVE. Exhaustive exercise also modulated tissue antioxidant enzymes. CONCLUSIONS: Vitamin E supplementation markedly decreased fish oil induced antioxidant enzyme activities in all tissues. Sparing of glutathione may be an important mechanism by which vitamin E decreased tissue protein oxidative damage.     

Effect of vitamin E supplementation on hypoxia-induced oxidative damage in male albino rats

BACKGROUND: There is growing evidence that free radicals mediated oxidative injury due to inadequate oxygen availability is an important factor in various pathologies at high altitude. Since vitamin E is known to protect the cells from oxidative damage due to its potent antioxidant properties, the present study was carried out to explore the effect of vitamin E supplementation on various hematological and biochemical parameters in hypoxia-induced oxidative stress in albino rats. METHODS: The experiments were conducted on male albino rats by intermittently exposing them to a simulated altitude of 7,576 m (25,000 ft), daily for 6 h for 15 d at 32 +/- 2 degrees C. The control group was fed vehicle only (1% Tween 80) and the experimental group was given vitamin E (40 mg per rat x d(-1)) orally, 5 d prior to and during the period of hypoxic exposure. The variables studied include: hemoglobin, hematocrit, RBC deformability index, alpha-tocopherol level, malondialdehyde (MDA), reduced glutathione (GSH), oxidized glutathione (GSSG), lactate dehydrogenase (LDH) and protein level in blood/plasma and various tissues. RESULTS: Significant increase in hematocrit and hemoglobin and decrease in RBC deformability index was observed on exposure to hypoxia while vitamin E supplementation maintained them at the normal level. Hypoxia led to the decrease in plasma vitamin E and blood glutathione (GSH) level and two-fold increase in the plasma malondialdehyde (MDA) level. Vitamin E supplementation, on the other hand, resulted in less of an increase in MDA and increased the GSH concentration significantly. LDH activity, which was elevated on exposure to hypoxia, was arrested on vitamin E supplementation. CONCLUSION: The results indicate that vitamin E supplementation results in preventing oxidative damage due to high altitude stress.     

Effect of dietary "antioxidant" supplementation on the susceptibility to oxygen toxicity in mice.

This study was undertaken to test chronic feeding of some normal dietary constituents on susceptibility to oxygen toxicity. Eight-week-old male CD-1 mice were fed a semi-purified diet simulating that of the average American male and supplemented with either vitamin E, vitamin K3, selenium, or the sulfur amino acids methionine and cystine. After 2, 4, 8, or 16 weeks, groups of mice were exposed to oxygen at 1, 4, or 8 ATA and times to respiratory distress, convulsion, and death recorded. Vitamin E and amino acid supplementation had no effect whereas vitamin K and selenium supplements increased time to death at 1 ATA. Only the effect of selenium was statistically significant. All diets significantly increased the time of onset of the measured parameters beginning after 4 weeks, suggesting that one or more constituents of the basal diet afforded some protection against oxygen toxicity.     

维生素E对血液透析病人氧化应激的干预效果

目的　研究抗氧化剂维生素E对血液透析病人氧化应激状态的干预效果。方法　处于稳定状态的血液透析病人 5 6例 (不服用任何抗氧化药)采用自身对照的方法 ,观察 1个月后 ,随机均分为两个实验组 ,A组口服维生素E 2 0 0mg/d ,B组口服维生素E 4 0 0mg/d,服药 1个月 ;两组分别在观察期和服用维生素E干预期前后检测循环晚期氧化蛋白产物(AOPP)、丙二醛 (MDA)和谷胱甘肽过氧化物酶(GSHPx)水平以及血清维生素E浓度。另选 5 6例健康者作为正常对照组。结果　实验组血清AOPP、MDA水平明显高于同龄正常对照组(n =5 6 ,P <0 0 1) ,GSHPx、维生素E浓度明显低于正常人(P <0 0 1) ;透析病人在未服抗氧化药的 1个月观察期前后AOPP、MDA、GSHPx及维生素E浓度无明显变化 (P均 >0 0 5 ) ;A组治疗后 ,血清维生素E水平较治疗前明显增高 (P <0 0 1) ,但AOPP、MDA和GSHPx水平与治疗前相比无明显差异 ;B组治疗后血清维生素E、GSHPx水平较治疗前增高 (P <0 0 1,P <0 0 5 ) ,AOPP较治疗前明显降低 (P <0 0 1) ,但MDA水平无明显变化。结论　口服大剂量维生素E(4 0 0mg/d)可以改善血透病人的氧化应激状态 ;血透病人短期服用大剂量维生素E未见明显副作用。     

等幅正弦中频电流对急性低压缺氧小鼠学习记忆障碍的影响

目的：探讨等幅正弦中频电疗法对急性低压缺氧引起的学习记忆障碍是否有保护作用。方法：72只小鼠随机分为4组：对照组,缺氧组,电疗组,电疗＋缺氧组。用小鼠跳台、避暗实验法,观察各组小鼠学习记忆功能。用电镜观察急性低压缺氧及等幅正弦中频电疗后,脑皮质细胞形态学改变。结果：跳台实验与避暗实验表明：电疗法＋缺氧组与缺氧组相比,错误次数（M）明显减少。等幅正弦中频电疗法可缓解因缺氧导致的神经元的核变形、核膜结构不光滑以及细胞器数量减少等现象。结论：等幅正弦中频电流的预防性治疗,可改善由低压缺氧造成的记忆功能损害,并对急性缺氧的脑神经元具有保护作用。     

Lipid metabolic indices in man during head-down tilt hypokinesia and their correction

Twenty one test subjects exposed to head-down tilt for 120 days were subdivided to four groups: Group 1--nine subjects used as controls, Group 2--three bed rested subjects who performed regular exercises, Group 3--four bed rested subjects who were given selected drugs, including Vitamin F-99 that influenced lipid metabolism, and Group 4--four bed rested subjects who performed regular exercises and received Vitamin F-99. At different stages of bed rest and recovery the content of lipoprotein fractions and lipids of different classes in serum was measured by thin-layer chromatography. The concentration of cholesterol in biliary lipids was determined. In Group 1 and 2 subjects bed rest led to a drastic and significant increase of cholesterol esters in blood, a decrease of phospholipids, variations of triglycerides and non-esterified fatty acids, and a lower percentage content of alpha-lipoproteins. The use of Vitamin F-99 produced positive changes in the above parameters of lipid metabolism (it normalized the level of cholesterol and phospholipids). In Group 4 subjects the effect of exercise combined with drugs was most distinct.     

针刺关冲对急性缺氧小鼠能量代谢的影响

目的：观察针刺关冲能否改善急性缺氧小鼠的能量代谢。方法：将36只小白鼠平均分成关冲、缺氧对照、空白对照三组，以Na^＋-K^＋ATPase和LDH活性为指标，观察针刺关冲对急性缺氧20min小白鼠大脑皮层、心肌能量代谢影响的差异。结果：关冲组大脑皮层、心肌Na^＋-K^＋ATPase、LDH活性与缺氧对照组比较均有显著性升高（P〈0．05）。结论：针刺关冲能改善急性缺氧小白鼠的能量代谢，其机理可能与针刺提高大脑皮层、心肌Na^＋-K^＋ATPase、LDH活性有关。     

维生素D预防儿童急性呼吸道感染诱导哮喘发作的研究

目的：研究维生素D对于儿童急性呼吸道感染诱导哮喘发作的预防效果及安全性。方法选择2009年11月～2013年5月收治的188例哮喘缓解期患儿作为研究对象,将所有患儿按照随机分组原则分为试验组A （94例）与试验组B（94例）,两组患者均采用常规缓解哮喘药物,试验组B除上述治疗外哮喘发作前不予任何干预,试验组A在上述基础上每日服用罗钙全胶囊作为预防措施,两组随访2周观察随访期间哮喘发作情况,比较哮喘发作严重程度。另外选取30例体检健康的儿童作为对照,检测治疗前所有患者的维生素D水平及对照组维生素D水平,比较治疗前、后维生素D水平差异。结果试验组A哮喘发作者24例,其中轻度18例,中度6例,无重度者;试验组B哮喘发作56例,其中轻度24例,中度21例,重度9例;两组发病率具有显著差异性,P＜0.05;治疗前试验组A、B维生素D水平无显著差异同对照组相比显著低,治疗后试验组A维生素D水平显著上升,同对照组无明显差异性,试验组B同治疗前无明显变化。结论维生素D水平的缺乏可能是哮喘的重要原因,通过积极补充维生素D水平可以降低急性呼吸道感染诱发哮喘发作的发病率。