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Breviscapine the role of anti-cerebral hypoxia in mice_832

By Troy Graham,2014-10-30 11:34
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Breviscapine the role of anti-cerebral hypoxia in mice_832

Breviscapine the role of anti-cerebral hypoxia in mice

     Abstract Objective To study the Breviscapine

    (Breviscapine) on the protective effect of cerebral hypoxia in mice. Method 10,20 mg / kg fed continuously Breviscapine (Intragastric infusion, ig) mice 7 d, mice in each group were injected intraperitoneally (Introperitoneal injection, ip) 200 mg / kg NaNO2 or decapitation, record mouse ip After the survival time and decapitated NaNO2 after the duration of mouth breathing. The results of 10,20 mg / kg Breviscapine to make ip 200 mg / kg NaNO2 mice survived longer than the control group extension of 83.9%, and 4.93%; 10,20 mg / kg dose group breviscapine two mice decapitated The duration of post-mouth breathing is a blank control group were 1.60 and

    1.30 times. Conclusion Breviscapine mice ip NaNO2 and breakage caused by cerebral hypoxia has a protective effect.

     Key words Breviscapine Cerebral anoxia

     Protective Effects of Breviscapine on Cerebral Hypoxia in Mice

     Abstract: ObjectiveTo study the protective effects of breviscapine on cerebral hypoxia in mice. MethodsThe protective effects on cerebral hypoxia were investigated on survival time after ip 200 mg / kg NaNO2 and gasping duration after decapitation in mice following 7d consecutive oral

    administration of breviscapine (10, 20 mg / kg, ig). ResultsAdministration of breviscapine (10 mg / kg, ig) for 7 d could significantly prolong survival time after ip NaNO2 in mice.Compared with control group, the survival time after ip

    NaNO2 was prolonged 83.9% and 4.93 %. Administration of breviscapine (10,20 mg / kg, ip) for 7d could significantly prolong gasping duration after decapitation in mice. The

    gasping duration after decapitation of the two experiment groups were found 1.60 and 1.30 times of the control group respectively. ConclusionBreviscapine has significant protective effects on cerebral hypoxia in mice.

     Key words: Breviscapine; Cerebral hypoxia

     Breviscapine (Breviscapine) is from the short-ting

    Erigeron Asteraceae Erigeron species isolated from the whole plant flavonoids, the active ingredient is scutellarin yuan for the mother nucleus, and its molecular structure was baicalin C4 spaces connected to a hydroxyl, is a prime and Breviscapine scutellarin mixture to scutellarin-based [1].

    Currently, the study breviscapine focused on the cardiovascular and cerebrovascular diseases, pharmacology study found that breviscapine able to increase cerebral blood flow and reduce vascular resistance, lower blood viscosity;

    clinic for the treatment of brain Breviscapine infarction, hemiplegia after stroke, coronary heart disease, angina pectoris, total effective rate was 90% [2]; its security agents over large areas, and few adverse reaction [3]. Breviscapine on neurovascular disease and effective, but the role of hypoxia-induced nerve damage have not been reported. The experiments were carried out on mice ip NaNO2 and decapitated treatment of acute toxic hypoxia and complete ischemia and hypoxia model to explore breviscapine protective

    effect of cerebral hypoxia in mice.

     1 Materials and methods

     1.1 Materials

     23 ~ 25 g Kunming mice, male and female in half, Experimental Animal Center of our hospital; Breviscapine: Wang Yuxi, Yunnan Province, Bio-Pharmaceutical Co., Ltd. to provide sub-Lung; NaNO2 AR: Tianjin Chemical Reagent Factory production Beichen Hua Yue.

     1.2 Methods

     1.2.1 ip NaNO2 acute hypoxia experiment 24 mice were randomly divided into 3 groups, each group of mice were continuously ig Breviscapine (10,20 mg / kg) 7 d, the control group ig an equal volume of distilled water, 1 h after the

    last administration each group mice were ip NaNO2 200 mg / kg, recording the time of death in mice.

     1.2.2 decapitation ischemia and hypoxia in mice

    experiments 24 mice were randomly divided into three groups, each group of mice were continuously ip Breviscapine (10,20 mg / kg) 7 d, control group ip equal volume of distilled water, at the end times to the drug 1 h after the mice in each group

    along the ears decapitation, mice were decapitated after recording the duration of mouth breathing (in mice exposed tongue and mouth breathing stops and the marked stop the clock).

     2 Results

     2.1 Breviscapine on survival time of mice ip NaNO2 the

    impact of 10,20 mg / kg Breviscapine groups of mice ip NaNO2 200 mg / kg survival time after the saline control group, respectively 1.11,1.04 times (see Table 1), and 10 mg / kg Breviscapine role in more than 20 mg / kg Breviscapine role. Table 1 Breviscapine on survival time of mice after ip NaNO2 effects (abbreviated)

     2.2 Breviscapine panting after decapitation of mice the duration of the impact of 10,20 mg / kg Breviscapine panting after decapitation of mice than the saline control group, the

    duration of extension of 59.72% and 29.86% (see Table 2), and found that 10 mg / kg Breviscapine role in more than 20 mg / kg Breviscapine role. Table 2 Breviscapine panting in mice after decapitation of time effects (abbreviated)

     3 Discussion

     Cerebral hypoxia, ischemia is caused by many neurological diseases, the main reason for decreased in the nerve ischemic / hypoxic injury, involving a very complex mechanism of neuronal damage and death, including neuronal energy failure, excitotoxicity injury, intracellular calcium overload-mediated

    damage, cell protease-activated, the release of free fatty

    acids as well as the formation of free radicals and so on, with both inflammatory mediators caused by local inflammatory reactions and ischemia and neuronal injury after hypoxia is

    closely related to [4] . Understanding of ischemic / hypoxic neurological damage resulting from elaboration of its

    mechanism is very necessary, any reduction in cerebral hypoxia / ischemia injury measures indicate on the treatment of

    neurological diseases, impaired possible. Reposted elsewhere in the paper for free download http://

     In laboratory studies, large doses of NaNO2 and decapitated as a common model to simulate the clinical cerebral hypoxia / ischemia resulting from impaired

    neurological diseases [5]. NaNO2, after entering the body, resulting in high hemoglobin hyperlipidemia, so that heme iron in the form of high-speed railway, while the latter is easily combined with hydroxyl firm can not be converted to ferrous

    hemoglobin, and thus can not transport oxygen, causing brain and systemic hypoxia , energy supply disruption [6], nervous system, the demand for oxygen and energy is very sensitive in comparison with other organizations, brain tissue oxygen consumption high, and there is no energy storage in brain tissue [7], so the brain cells under hypoxia GABA, DA and the concentration of amino acid neurotransmitters such as imbalance, the brain acetylcholine synthesis and release of reduced free radical production increased neuronal plasticity

    changes and nerve cell necrosis, thus affecting the nervous system function [8]. Sleepy complete cerebral ischemia also experienced a similar or more acute cerebral hypoxia, lactate / pyruvate ratio increased rapidly, NAD bank balance, the

    results also led to cerebral energy metabolism disorder. At the same time, Na +, Ca2 + influx rapidly, cell excitability increased, more emphasis on drug and energy depletion of cells to accelerate the death of nerve cells, causing neurological

    disorders [5]. In this study, using mice with high-dose ip

    NaNO2 and decapitated hypoxia model checking of anti-hypoxia

    effect Breviscapine. Breviscapine short-ting from the

    Asteraceae Erigeron Erigeron species isolated from the whole plant flavonoids, with expansion of heart and brain blood vessels, lowering blood viscosity and other pharmacological effect, its main role of the mechanism is Breviscapine can reduce cerebral edema, increased Na +-K +-ATPase and Ca2 +-

    ATPase activity and inhibit neuronal Na +, Ca2 + influx

    induced cell excitability; regulation of intracellular ATP, glucose, amino acids, the concentration of imbalance, lower cytotoxicity and energy depletion, to reduce cell death [9,10]. At the same time, can significantly reduce the breviscapine ischemic / hypoxic nerve cells in marginal zone apoptosis inhibitory protein kinase activity, regulation of

    cell signal transduction, regulation of neurotransmitter release and gene expression, especially for the nervous system regulating free radicals effect [11], there are beneficial for neuronal injury, thereby restoring the nervous system structure and function.

     The experimental results show that Breviscapine can prolong the survival time of mice after ip NaNO2 and decapitated after the open mouth breathing time showed acute toxic hypoxia and complete ischemia / hypoxia against the role of such a confrontation breviscapine effect may be related to regulating ATPase activity and inhibit neuronal Ca2 + overload caused by excitotoxicity and lipid peroxidation, inhibit

    protein kinase activity, regulation of cell signal transduction, regulation of neurotransmitter release and gene expression in a variety of factors, but through these mechanisms are conducive to a variety of hypoxic damage to improve neurological function.

     In this study, selection of a continuous ig 10,20 mg / kg Breviscapine 7 d to test its anti-hypoxic effect The effect of

    two doses of the two models in parallel, and 10 mg / kg of anti-hypoxia Breviscapine the role of valence is higher than

    20 mg / kg, the results often appear the role of traditional Chinese medicine extracts The effect of inverted U-consistent,

    specific anti-cerebral anoxia can play the lowest effective dose also need to be further explored.

     References

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     [2] Cui Jianmei, Woosung. Breviscapine Research progress [J]. Natural Product Research and Development, 2003,15 (3): 255.

     [3] Lin Xiong, Chu Kdan. Breviscapine pharmacological research [J]. Strait of Medicine, 2005,17 (6): 5.

     [4] Mei-Yu Geng, Xin Xian-Liang, Li Jing, et al.

    Pathogenesis of cerebral ischemia and drug treatment [A].

    ZHANG Jun-Tian. Neuropharmacology research [M]. Beijing: People's Health Press, 2002:66.

     [5] by Ya-zhen, Cai Zhenling, Meng Yan-Bin, et al. Huang

    TF pairs of protective effect of cerebral hypoxia in mice [J]. Chengde Medical Journal, 2001,18 (1): 5.

     [6] Qin Cai, Zhang Jun-Tian. Nimodipine, nifedipine and Changchun amine chemical-related memory impairment in mice to improve the role of [J]. Chinese Academy of Medical Sciences Journal, 1986,8 (5): 366.

     [7] Ames 3rd A. CNS energy metabolism as related to function [J]. Brain Res Brain Res Rev 2000,34: 42.

     [8] Wan Hai Tong, Wang. Breviscapine treatment of cerebral ischemia of the research [J]. Zhejiang Journal of Traditional Chinese Medicine, 2006,30 (1): 101.

     [9] Zhang Yan, Chen Qun, GU, et al. Erigeron on ischemia-

    reperfusion in gerbil hippocampal ATP concentration change and the impact of the release of excitatory amino acids [J]. Jiangsu Medicine, 2005,31 (11): 843 .

     [10] Liao Wei Jing, Yang Yun Huang, Fan. Breviscapini

    agents on ischemic brain injury in the early reperfusion of brain imaging and the role of neural metabolites [J]. Chinese Journal of Traditional Chinese Medicine, 2003,28 (2): 163.

     [11] Xiao-Bing Zhang, Peng-generation silver, Chu Man-

    fang, et al. Breviscapine pills on focal cerebral ischemia-

    reperfusion injury in rats [J]. Anhui Traditional Chinese Medical Journal, 2003,22 (1): 45. reposted elsewhere in the paper for free download http://

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