中药抗辐射作用的研究进展

电离辐射导致机体出现各种损伤,包括氧化应激损伤、造血系统的功能异常、免疫功能障碍及细胞DNA链断裂等,辐射的危害已不容忽视。因此,研究开发抗辐射损伤的药物,特别是中药抗辐射损伤活性成分的研究,在现代医药保健事业中受到人们的极大关注。研究发现很多中药具有明显的清除自由基、保护造血系统和增强机体免疫的作用,因此能保护机体免受辐射损伤,且毒副作用小,是较好的辐射防护剂。该文分别简要综述中药复方、单味中药、中药有效成分抗辐射作用的研究进展。     

姬松茸多糖对辐射损伤大鼠的免疫调节作用

<正>辐射可引起机体物质代谢紊乱、造成机体免疫系统损伤,还会引起机体多种器官的氧化损伤,使体内防御系统被严重破坏~([1])。目前一些效果明显抗辐射药物往往因其不良反应较大无法广泛应用~([2]),研究利用纯天然植物中的活性成分提高机体抗辐射能力,预防和减轻辐射对机体的损害逐渐成     

四气五味的中药抗辐射防护作用的机理探讨

中药的药性主要核心为四气五味,并且许多中药具有良好的抗辐射防护作用,但目前临床上对中药抗辐射的机理尚不清楚,需要进一步的研究,因此,笔者对目前临床对中药抗辐射防护作用的研究进行分析,以探讨中药抗辐射防护作用的机理。     

中药抗辐射作用的研究进展

随着科学技术的现代化，核能日益广泛地应用于生产、科研、医疗以及日常生活中，辐射在给人们造福的同时，也带来越来越多的不利影响。据报道，肿瘤患者约有70％是采用放射治疗，但放疗在杀死肿瘤细胞的同时，也对机体的正常组织造成损伤，从事放射性职业的工作者也会受到一定程度的辐射损害。因此，研制抗辐射药物很有意义。经过多年的研究，人们发现具有清热解毒、活血化瘀、补血益气、养阴升白的中药均有不同程度的抗辐射作用，且中药药源广、毒性低，使其在辐射防护剂的研究中显示出巨大的优势和潜力。现将近年来的中药抗辐射研究作一概述。     

抗辐射损伤药物的研究进展

近年来人们接受的辐射越来越多,辐射损伤已成为威胁人类健康的潜在因素。为减轻损伤所致的危害,抗辐射损伤药物的研发任重道远。目前市场上逐渐涌现出一系列具有较好保护效应的抗辐射损伤药物,但部分药物存在着不容忽视的副作用,因此发现新型高效低毒的辐射保护剂迫在眉睫。本文就辐射损伤危害及抗辐射药物的研究现状进行综述,为进一步新药开发提供理论依据及指导。     

抗辐射天然产物研究进展

随着科技的高速发展,基于核物理的诊断技术和放疗技术在医学中得到广泛应用,但同时也会给人体造成不同程度的损伤。因此,研究和开发能够预防以及治疗辐射损伤的药物意义重大。综述抗辐射天然产物如多糖、黄酮、酚酸、皂苷等的研究进展,并对其研究前景进行展望,为其进一步开发提供参考。     

玉屏风散对慢性氟中毒大鼠抗氧化作用的影响

本文以慢性氟中毒大鼠作为模型,研究氟对机体抗氧化作用的影响,以及中药玉屏风散对机体的保护作用,为探索氟中毒的损伤机制及如何预防、减轻氟对机体的损伤作用提供实验依据.     

麦冬皂苷药理作用研究进展

麦冬作为一种滋阴药,在传统中药中占有重要地位。随着对麦冬研究的不断深入,其主要有效成分皂苷类的药理活性也不断被发现。综述近年来麦冬皂苷在抗心脑血管疾病、抗衰老、改善学习记忆障碍、抗肿瘤、抗辐射、抗炎、免疫调节、镇咳、改善肝肺病理性损伤等方面的药理作用研究进展,以期为今后对麦冬及其皂苷类活性成分的深入研究和开发利用提供参考。     

两种不同产地螺旋藻抗辐射功能的比较

随着核能和核技术应用的日益广泛，人群接受低剂量长期电离辐射已越来越严重，仅靠避免接触或物理防护来消除辐射的危害是被动的，而人群长期摄入抗辐射保健食品是一种积极有效的方法。目前，国内保健品市场上宣传抗辐射功能的主要产品是螺旋藻，但因藻种属及培养条件的不...     

中药黄芪的药理作用及临床应用效果观察

目的探讨中药黄芪的药理作用及其临床应用效果。方法回顾性分析我院应用中药黄芪的临床资料,观察其临床效果。结果中药黄芪在治疗心肌梗死、心力衰竭、脑血栓、糖尿病肾病等方面具有独特作用,疗效明显。结论中药黄芪具有增强细胞免疫功能、抗辐射及抗感染等作用,值得临床研究和应用。     

Naloxone benzylhydrazone is a µ-selective opioid antagonist without kappa agonist effects in rhesus monkeys

Naloxone benzoylhydrazone (NalBzoH) has been suggested to be a selective opioid agonist, exerting its effects through the kappa(3) subtype of opioid receptor. In the present experiments NalBzoH was studied for its discriminative stimulus, analgesic, and respiratory effects in rhesus monkeys. Up to the largest doses administered (1.0-3.2mg/kg), NalBzoH failed to substitute for the discriminative stimulus effects of the kappa agonist ethylketocyclazocine or those of the μ agonist alfentanil. However, in morphine-treated (3.2mg/kg/day) monkeys NalBzoH substituted completely for the discriminative stimulus effects of the opioid antagonist naltrexone. NalBzoH antagonized the discriminative stimulus effects of alfentanil in morphine-treated subjects and, at larger doses, antagonized the discriminative stimulus effects of ethylketocyclazocine. NalBzoH did not produce analgesic effects and had only modest effects on respiration. However, NalBzoH antagonized the analgesic effects as well as the respiratory-depressant effects of alfentanil; at doses 10-15 times larger than those that antagonized alfentanil, NalBzoH also antagonized analgesic effects of the kappa agonist U-50,488. For both μ and kappa agonists, NalBzoH was slightly more potent in antagonizing discriminative stimulus effects as compared to analgesic effects. Thus, NalBzoH is a μ-selective opioid antagonist in rhesus monkeys and is equipotent to naloxone in antagonizing alfentanil. While demonstrating μ-selective antagonism, the current study fails to provide support for the proposed kappa agonist actions of NalBzoH.     

Carry-over effects in bioequivalence studies.

Carry-over effects are often considered to be one of the main problems of the cross-over design: should we adjust for carry-over or not? We attempt to answer this question by examining the observed frequency of carry-over effects in actual bioequivalence studies. A total of 96 six-sequence, three-period, three-treatment fed-fasted studies are analyzed for carry-over effects and 324 two-sequence, two-period, two-treatment fasted studies are analyzed indirectly for carry-over effects via sequence effects. Two log-transformed pharmacokinetic variables, Cmax and AUC0-t, are modeled in an analysis of variance. The impact of statistically significant carry-over effects on bioequivalence results is examined and the rationale behind not adjusting for carry-over in bioequivalence studies is discussed.     

Acute and chronic effects of alcohol use on violence

While the empirical association of drinking and problem drinking to violence is well established, the etiological nature of the relationship is poorly understood. Using data collected from 1,149 convicted male felons, the acute (drinking just before the violent event) and chronic (a psychiatric diagnosis of alcohol abuse or dependence) effects of alcohol use on violence were analyzed. Logistic regression models were used to examine the relationship of acute and chronic alcohol effects to incarceration for a violent offense and arrest for a violent offense, with demographic and criminal history factors controlled. The acute effects of alcohol were found to be significantly associated with incarceration for a violent offense, but the net explanatory capacity of acute alcohol effects was not large. Chronic alcohol effects were not significantly associated with incarceration for a violent offense or arrest for a violent offense in the previous year. The findings were interpreted as being consistent with the hypothesis that alcohol effects violence directly, acting through the acute effects of use, rather than indirectly through the effects of underlying or mediating factors.     

Attenuation of the stimulant and convulsant effects of cocaine by 17-substituted-3-hydroxy and 3-alkoxy derivatives of dextromethorphan

Pharmacological evidence has suggested a role for both sigma and N-methyl-D-aspartate (NMDA) receptors in the behavioral stimulant effects of cocaine and its convulsant effects observed at higher doses. A series of dextromethorphan (DM) analogs with a range of affinities for sigma-1 binding sites and for the NMDA receptor ion channel were used to explore the contribution of these two mechanisms in controlling the stimulant and convulsant effects of cocaine. These compounds were potent and efficacious blockers of both stimulant and convulsant effects produced by acute cocaine administration in mice (cocaine 10 or 75 mg/kg ip for locomotor activity or convulsions, respectively). Generally, the DM analogs blocked these effects of cocaine at doses that did not display ataxic and sedative side effects as measured in the inverted screen test. In contrast to the high-affinity NMDA blockers, (+)-MK-801 (dizocilpine) and dextrorphan (DX), DM and analogs did not stimulate locomotor activity. There was no significant correlation between the affinities of the DM analogs for the sigma-1 or the phencyclidine (PCP) binding site and their potencies to produce behavioral effects on their own or to attenuate the behavioral or toxic effects of cocaine. The present study has identified a series of agents that have cocaine-blocking effects that appear to be distinct from that of classical sigma-1 receptor ligands and that of traditional uncompetitive NMDA receptor antagonists. These findings point to potentially novel pharmacological strategies for blocking cocaine stimulant and toxic effects.     

Desipramine potentiation of the acute depressant effects of ethanol: modulation by alpha2-adrenoreceptors and stress

Ethanol exerts effects on the brain noradrenergic system, and these are thought to contribute to the sedative/hypnotic (depressant) effects of ethanol. Recent studies suggest that the norepinephrine transporter (NET) plays an important role in modulating ethanol's depressant effects. The aim of the present study was to further characterize this role. Transporter blockers with varying affinity for NET versus the serotonin transporter (desipramine>fluoxetine>citalopram) were tested for their ability to alter ethanol's depressant effects, and for comparison, hypothermic effects. Effects of desipramine on another depressant, pentobarbital, were examined. Desipramine potentiation of ethanol's depressant effects was assessed following depletion of brain norepinephrine via N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (DSP-4) treatment, or depletion of brain 5-HT via para-chlorophenylalanine methyl ester hydrochloride (PCPA) treatment. The effects of co-administration of either the selective alpha2-adrenoreceptor agonist (dexmedetomidine) or the selective alpha2-adrenoreceptor antagonist (atipamezole) on desipramine's effect on ethanol's depressant effects were examined. Given the close link between stress, ethanol and norepinephrine, desipramine potentiation of ethanol's depressant effects was tested following repeated forced swim stress. Results showed that desipramine, but not SERT-selective doses of citalopram or fluoxetine, strongly potentiated the depressant (not hypothermic) effects of ethanol. These effects were mimicked by dexmedetomidine and blocked by atipamezole, but not by depletion of either norepinephrine or 5-HT. Desipramine potentiation of ethanol's depressant effects was abolished following repeated stress. Present findings further support a major role for NET and the alpha2-adrenoreceptor in modulating the depressant effects of ethanol, with possible implications for understanding the role of noradrenergic dysfunction in stress-related alcoholism.     

毒性试验组织病理学结果有害作用判断概述

药物非临床安全性评价毒性试验有害作用的判断非常重要,因其可为保护临床试验暴露于新化学实体或药物的受试者提供重要信息。毒性试验组织病理学检查可提供受试物毒性作用的形态学数据,帮助分析和确定有害作用和非有害作用及其剂量水平。参照美国毒性病理学会（STP）和欧洲毒性病理学会（ESTP）的推荐最佳实践或建议及其他相关文献,对有害作用的定义、区分有害作用与非有害作用的要素、有害作用数据沟通和使用来评估人类潜在风险等建议等进行简要概述分析,以期为我国非临床药物安全性评价毒性试验中有害作用判定提供参考。     

CARRY-OVER EFFECTS IN BIOEQUIVALENCE STUDIES

Carry-over effects are often considered to be one of the main problems of the cross-over design: should we adjust for carry-over or not? We attempt to answer this question by examining the observed frequency of carry-over effects in actual bioequivalence studies. A total of 96 six-sequence, three-period, three-treatment fed-fasted studies are analyzed for carry-over effects and 324 two-sequence, two-period, two-treatment fasted studies are analyzed indirectly for carry-over effects via sequence effects. Two log-transformed pharmacokinetic variables, C _max and AUC_0-t, are modeled in an analysis of variance. The impact of statistically significant carry-over effects on bioequivalence results is examined and the rationale behind not adjusting for carry-over in bioequivalence studies is discussed.     

Central nervous system effects of the imidazodiazepine Ro 15-4513

Ligands for benzodiazepine receptors produce one of three types of effects: (1) diazepamlike; (2) opposite to diazepam; or (3) no direct effects, but blockade of the effects of the other ligands. Data refiewed in this paper demonstrate that the imidazodiazepine Ro 15-4513 produces direct neuronal and behavioral effects of the type opposite to those of diazepam. These include electrophysiological and behavioural seizures, anxiety-like behaviors, inhibition of aggression, and facilitation of learning and memory. In addition to its direct effects, Ro 15-4513 also blocks the effects of benzodiazepines, barbiturates, and ethanol. This antagonism has been reported for a broad range of experimental approaches including biochemical, physiological, and behavioral measures. Because direct effects of Ro 15-4513 are, in many cases, opposite to the effects of these sedative drugs, these direct effects may account for at least part of the ability of Ro 15-4513 to antagonize sedative drugs. However, for some measures, such as exploratory activity and operant response rate, even under conditions in which the effect of Ro 15-4513 is the same as that of the sedative drugs, Ro 15-4513 still antagonizes the effects of the sedative drugs. Blockade of the effects of Ro 15-4513 by both agonists and antagonists at the benzodiazepine receptor strongly supports the hypothesis that all of the effects of Ro 15-4513 occur due to its action at the benzodiazepine receptor. Blockade of ethanol by very low concentrations of Ro 15-4513 substantiates the role of the benzodiazepine receptor-chloride ionophore complex in mediating neurobiological effects of ethanol and has stimulated efforts to develop alcohol antagonists with greater specificity and selectivity.     

Neurotoxic pesticides and behavioural effects upon birds

Organochlorine, organophosphorus, carbamate, pyrethroid and neonicotinoid insecticides and organomercury fungicides are all neurotoxic and therefore have the potential to cause behavioural disturbances in birds. A number of studies have described behavioural effects caused to captive birds by neurotoxic pesticides, but it is very difficult to measure such effects in the field, which is a serous limitation given their potential to cause adverse effects at the population level. The mode of action, and the neurotoxic and behavioural effects of these compounds are briefly reviewed before considering evidence for their effects in the laboratory and field. Behavioural effects may cause adverse changes at the population level either directly or indirectly. Direct effects upon avian populations may be due to disturbances of reproduction, feeding, or avoidance of predation. Indirect effects on predators may be the consequence of direct action upon the prey population leading to either (1) reduction of numbers of the prey population, or (2) selective predation by the predator upon the most contaminated individuals within the prey population.Attention is given to the historic evidence for neurotoxic and behavioural effects of persistent organochlorine insecticides, raising the question of retrospective analysis of existing data for this once important and intensively studied class of compounds. Less persistent pesticides currently in use may also have neurotoxic effects upon birds in the field. Sometimes, as with some OPs, their effects may outlast the persistence of their residues, and the ecotoxicity and persistence of some may be affected by interactions with other environmental chemicals. The development of new mechanistic biomarker assays could improve understanding of behavioural effects and possible associated effects at the population level caused by such compounds in the field.     

Discriminative stimulus effects of ethanol with a conditioned taste aversion procedure: lack of acetaldehyde substitution

Acetaldehyde has been suggested to mediate a number of the pharmacological and behavioural effects of ethanol. Recently, several studies investigated the role of acetaldehyde in the subjective effects of ethanol, but obtained conflicting results. With the discriminative taste aversion (DTA) procedure, high acetaldehyde doses were shown to substitute for the discriminative stimulus effects of ethanol. In contrast, the operant drug discrimination protocol failed to show any substitution effect of acetaldehyde. Several methodological differences between the two procedures could explain these discrepancies, and particularly the absence of an individual discrimination criterion in the DTA procedure. In the present study, the DTA procedure was adapted to introduce such a criterion. In addition, the effects of acetaldehyde were compared with those of other drugs, for which the substitution effects for ethanol are well known. Rats were trained to discriminate 1.0 g/kg ethanol from saline in a DTA protocol. When the rats met the criterion of ethanol discrimination, various doses of several drugs were tested for their ethanol stimulus substitution effects: ethanol, acetaldehyde, dizocilpine, diazepam and nicotine. The results showed a clear dose-dependent discrimination of ethanol stimulus effects. In addition, dizocilpine fully substituted for ethanol, while diazepam only partially substituted. In contrast, both acetaldehyde and nicotine failed to substitute for ethanol. These results show that acetaldehyde is not significantly involved in the subjective and discriminative stimulus effects of ethanol. Acetaldehyde up to toxic doses did not substitute for the ethanol discriminative stimulus in the DTA protocol, when non-specific effects were carefully controlled.