發(fā)布時(shí)間：2017-12-30 19:08

  本文關(guān)鍵詞：非基因毒應(yīng)激對(duì)小G蛋白R(shí)hoB表達(dá)的誘導(dǎo)作用、機(jī)制及生物學(xué)意義　出處：《第二軍醫(yī)大學(xué)》2008年博士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 熱應(yīng)激 燙傷 缺氧 小G蛋白R(shí)hoB 細(xì)胞凋亡 p38 MAPK

【摘要】： 應(yīng)激是機(jī)體處于不利環(huán)境和遇到有害刺激時(shí)所產(chǎn)生的防御或適應(yīng)性反應(yīng),應(yīng)激反應(yīng)發(fā)生在整體和細(xì)胞層面,后者也稱為細(xì)胞應(yīng)激。糖皮質(zhì)激素(GC)是體內(nèi)最重要的應(yīng)激激素,其作用主要是由糖皮質(zhì)激素受體(GR)介導(dǎo)的,應(yīng)激時(shí)GC分泌增多對(duì)機(jī)體抵抗有害刺激起著極為重要的作用。動(dòng)物實(shí)驗(yàn)表明,切除雙側(cè)腎上腺后,極小的有害刺激即可導(dǎo)致動(dòng)物死亡,動(dòng)物幾乎不能適應(yīng)任何應(yīng)激環(huán)境。除了在整體應(yīng)激中發(fā)揮重要作用(如調(diào)節(jié)代謝、通過允許作用調(diào)節(jié)血壓等)外,已有較多體外實(shí)驗(yàn)顯示,GC能夠保護(hù)多種細(xì)胞免受應(yīng)激原所致的損傷和凋亡,受GC/GR調(diào)節(jié)的蛋白在此過程中可能發(fā)揮了重要作用,如已證明一些能被細(xì)胞應(yīng)激誘導(dǎo)、并在細(xì)胞應(yīng)激中發(fā)揮重要作用的應(yīng)激蛋白,如熱休克蛋白70,也能被GC/GR誘導(dǎo)。小G蛋白R(shí)hoB是近年來我們發(fā)現(xiàn)的一個(gè)新的GC/GR誘導(dǎo)蛋白。國外近年來的研究表明,RhoB是一個(gè)早期反應(yīng)基因,能夠被多種基因毒應(yīng)激原(致DNA損傷),如放射線、紫外線、抗癌藥(如5-氟脲嘧啶、順鉑)等誘導(dǎo)或使其激活,并有報(bào)道RhoB上調(diào)能夠促進(jìn)細(xì)胞存活。但是非基因毒應(yīng)激是否也影響RhoB的表達(dá)尚不十分清楚�？紤]到RhoB是GR調(diào)節(jié)蛋白,因此推測(cè)該蛋白有可能也在非基因毒應(yīng)激中起作用,本課題從在體和離體兩個(gè)水平觀察了熱應(yīng)激和低氧應(yīng)激這兩種常見的非基因毒應(yīng)激對(duì)RhoB表達(dá)的影響,并進(jìn)一步研究了熱應(yīng)激影響RhoB表達(dá)的機(jī)制以及可能的生物學(xué)意義,以期為臨床燒傷、休克等疾病的救治提供新的靶點(diǎn)。 一、熱應(yīng)激對(duì)RhoB表達(dá)的誘導(dǎo)作用、機(jī)制及生物學(xué)意義 (一)熱應(yīng)激能誘導(dǎo)RhoB的表達(dá) 我們首先制備了30%體表面積Ⅲ度燙傷大鼠模型,采用半定量RT-PCR、Real-time PCR及Western blot方法檢測(cè)了大鼠肝和肺組織中RhoB mRNA及蛋白的表達(dá)情況。結(jié)果發(fā)現(xiàn),大鼠肝,肺組織中RhoB mRNA在燙傷后2h時(shí)即上調(diào),4h時(shí)達(dá)到最大值,分別為對(duì)照組的7.5及5.7倍(p＜0.01);RhoB蛋白在燙傷后8h表達(dá)量最高。 由于燙傷后體內(nèi)會(huì)產(chǎn)生一系列的神經(jīng)內(nèi)分泌反應(yīng),而我們以往的實(shí)驗(yàn)也證實(shí)GC可以誘導(dǎo)RhoB的表達(dá)。為排除體內(nèi)的神經(jīng)內(nèi)分泌因素的影響,確定熱應(yīng)激本身是否可直接上調(diào)RhoB,我們進(jìn)一步觀察了熱應(yīng)激對(duì)體外培養(yǎng)的細(xì)胞中RhoB表達(dá)的影響。與整體實(shí)驗(yàn)采取肝、肺組織作為研究對(duì)象相對(duì)應(yīng),體外實(shí)驗(yàn)中選用了人肝癌HepG2細(xì)胞及人肺腺癌A549細(xì)胞;同時(shí)考慮肝、肺組織中除了實(shí)質(zhì)細(xì)胞以外,還含有大量的組織巨噬細(xì)胞,因此我們還選取了小鼠巨噬細(xì)胞系RAW264.7作為研究對(duì)象。結(jié)果顯示,熱應(yīng)激本身能以時(shí)間依賴性的方式快速地誘導(dǎo)這三種體外培養(yǎng)細(xì)胞中RhoBmRNA和蛋白的表達(dá)。上述實(shí)驗(yàn)表明,熱刺激在體內(nèi)和體外都可以上調(diào)RhoB的表達(dá),且這種誘導(dǎo)作用無明顯的組織細(xì)胞特異性。 (二)熱應(yīng)激誘導(dǎo)RhoB表達(dá)的機(jī)制研究 1.熱應(yīng)激上調(diào)RhoB mRNA的表達(dá)與增強(qiáng)其穩(wěn)定性有關(guān) 我們首先采用放線菌素D(5μg/ml)抑制基因的轉(zhuǎn)錄,觀察了熱應(yīng)激對(duì)RhoBmRNA穩(wěn)定性的影響,以明確熱應(yīng)激誘導(dǎo)RhoB的表達(dá)是發(fā)生在轉(zhuǎn)錄水平,還是在轉(zhuǎn)錄后水平。結(jié)果顯示,在A549細(xì)胞中熱應(yīng)激能使RhoB的半衰期由3.95h增加至7.1h(p＜0.01),在RAW264.7細(xì)胞中RhoB的半衰期則由3.98h增至7.6h(p＜0.01),表明熱應(yīng)激誘導(dǎo)RhoB mRNA的表達(dá)主要由RhoB的穩(wěn)定性增加所致。 2.應(yīng)激激活的p38 MAPK通路參與了熱應(yīng)激對(duì)RhoB的誘導(dǎo)作用。 已證實(shí)p38 MAPK信號(hào)通路能被包括熱應(yīng)激在內(nèi)的多種應(yīng)激原激活,我們因而觀察了p38 MAPK的抑制劑SB203580對(duì)熱應(yīng)激誘導(dǎo)RhoB表達(dá)的影響。結(jié)果顯示,于A549細(xì)胞的培養(yǎng)液中加入SB203580(10μM)抑制p38 MAPK的激活后,再將細(xì)胞進(jìn)行熱應(yīng)激處理,RhoB的誘導(dǎo)水平比未經(jīng)SB203580處理的細(xì)胞降低了約40%(p＜0.01);在RAW264.7細(xì)胞中RhoB的誘導(dǎo)水平降低了約50%(p＜0.01),表明p38 MAPK通路的激活參與了熱應(yīng)激對(duì)RhoB的誘導(dǎo)作用。 (三)熱應(yīng)激誘導(dǎo)RhoB表達(dá)的生物學(xué)意義及可能的機(jī)制 1.RhoB上調(diào)能夠抑制熱應(yīng)激誘導(dǎo)的細(xì)胞凋亡 應(yīng)激雖然是防御性反應(yīng),但嚴(yán)重的應(yīng)激也可導(dǎo)致細(xì)胞凋亡。因此,我們觀察了RhoB表達(dá)改變對(duì)A549細(xì)胞凋亡的影響,以探討熱應(yīng)激時(shí)RhoB上調(diào)的生物學(xué)意義。結(jié)果顯示,轉(zhuǎn)染RhoB野生型質(zhì)粒使RhoB過表達(dá)后,熱應(yīng)激引起的細(xì)胞凋亡比率由64.1%降至49.5%(p＜0.01),caspase3的活化也明顯降低;而利用RNA干擾的方法減少RhoB表達(dá)后,熱應(yīng)激引起的細(xì)胞凋亡比率以及caspase3的活化明顯增加,在RAW264.7細(xì)胞中也得到類似的結(jié)果,表明RhoB的上調(diào)能夠抑制熱應(yīng)激誘導(dǎo)的細(xì)胞凋亡。 2.RhoB上調(diào)抑制熱應(yīng)激誘導(dǎo)細(xì)胞凋亡的可能機(jī)制 (1)RhoB的上調(diào)能夠增強(qiáng)NF-κB的轉(zhuǎn)錄激活活性 已證明多種應(yīng)激原可激活轉(zhuǎn)錄因子NF-κB,激活的NF-κB通過調(diào)節(jié)多種基因的轉(zhuǎn)錄,調(diào)節(jié)細(xì)胞的生長(zhǎng)、分化、免疫和炎癥反應(yīng),并在應(yīng)激反應(yīng)中發(fā)揮重要作用,如已證明NF-κB在多種細(xì)胞中能抵抗多種應(yīng)激原導(dǎo)致的細(xì)胞凋亡。由此,我們進(jìn)一步觀察了RhoB對(duì)NF-κB轉(zhuǎn)錄激活活性的影響。結(jié)果顯示,在A549細(xì)胞及RAW264.7細(xì)胞中,瞬時(shí)轉(zhuǎn)染RhoB-wt質(zhì)粒使RhoB過表達(dá)后既可增加NF-κB的基礎(chǔ)轉(zhuǎn)錄激活活性,也可提高熱應(yīng)激時(shí)NF-κB的轉(zhuǎn)錄激活活性;而通過RNA干擾方法抑制RhoB表達(dá)后,則可明顯抑制NF-κB的轉(zhuǎn)錄激活活性。提示,RhoB的上調(diào)可能通過增強(qiáng)NF-κB的轉(zhuǎn)錄激活活性發(fā)揮抗凋亡的作用。 (2)熱應(yīng)激時(shí)RhoB的上調(diào)不影響熱休克蛋白70(HSPT0)的表達(dá) HSP70是一種可由熱及其他應(yīng)激原誘導(dǎo)產(chǎn)生的非特異性細(xì)胞保護(hù)蛋白,可以增強(qiáng)機(jī)體對(duì)應(yīng)激的耐受性,提高細(xì)胞生存率。大量研究表明,HSP70對(duì)射線(如γ-射線)、TNF-α等多種刺激誘導(dǎo)的細(xì)胞凋亡有抑制作用。因此,我們也觀察了RhoB表達(dá)的改變對(duì)HSP70表達(dá)的影響。在對(duì)A549細(xì)胞和RAW264.7細(xì)胞的研究中均發(fā)現(xiàn),無論是RhoB過表達(dá)還是通過RNA干擾方法使其表達(dá)受抑制,均不影響HSP70的表達(dá),表明HSP70并未參與RhoB對(duì)熱應(yīng)激誘導(dǎo)的細(xì)胞凋亡的抑制作用。 二、低氧對(duì)RhoB表達(dá)的誘導(dǎo)作用 我們首先將SD大鼠放入含8%O_2、92%N_2的混合氣體的低氧艙內(nèi)復(fù)制急性缺氧大鼠模型,采用Real-time PCR及Western blot方法檢測(cè)了大鼠脾臟和肺組織中RhoBmRNA及蛋白的表達(dá)情況。結(jié)果發(fā)現(xiàn),低氧能夠以時(shí)間依賴性方式誘導(dǎo)大鼠脾,肺組織中RhoB mRNA和蛋白的表達(dá)。繼而,我們又觀察了低氧對(duì)體外培養(yǎng)的人肺腺癌A549細(xì)胸及小鼠巨噬細(xì)胞系RAW264.7細(xì)胞中RhoB表達(dá)的影響。結(jié)果顯示,低氧本身也能夠以時(shí)間依賴性方式上調(diào)兩種細(xì)胞中RhoB mRNA和蛋白的表達(dá)。以上結(jié)果表明,低氧這個(gè)非基因毒應(yīng)激原也能夠在體內(nèi)和體外實(shí)驗(yàn)中誘導(dǎo)RhoB的表達(dá),且這種誘導(dǎo)作用沒有組織和細(xì)胞特異性。 綜上所述,本實(shí)驗(yàn)首次發(fā)現(xiàn),熱應(yīng)激、低氧這兩個(gè)非基因毒應(yīng)激原均能夠在整體水平和細(xì)胞水平誘導(dǎo)RhoB的表達(dá),且這種誘導(dǎo)沒有明顯的組織和細(xì)胞的特異性。熱應(yīng)激誘導(dǎo)RhoB的表達(dá)主要與其明顯提高RhoB mRNA的穩(wěn)定性有關(guān),而熱應(yīng)激時(shí)p38 MAPK通路激活參與了RhoB表達(dá)的上調(diào)。RhoB的上調(diào)能夠抑制熱應(yīng)激誘導(dǎo)的細(xì)胞凋亡,其機(jī)制并不是由HSP70介導(dǎo)的,而可能與RhoB增強(qiáng)NF-κB的轉(zhuǎn)錄激活活性有關(guān)。本課題所得的結(jié)果提示,RhoB具有細(xì)胞應(yīng)激蛋白的特征。
[Abstract]:Stress is the body in the unfavorable environment and have encountered harmful stimuli of defense or adaptive response, stress response and cell in the overall level, the latter is also known as cell stress. Glucocorticoid (GC) is the most important body of stress hormones, which is mainly composed of glucocorticoid receptor (GR) mediated when the stress, the increase of GC secretion of the body against harmful stimuli plays a very important role. The animal experiment showed that adrenalectomy, minimal harmful stimulation can lead to the death of the animal, the animal can hardly adapt to any environmental stress. In addition to play an important role in the overall stress (such as regulating metabolism, by allowing the effect of regulating blood pressure there have been many shows, etc.) in vitro, GC can protect cells from a variety of stressors caused by injury and apoptosis may play an important role in this process by regulating protein GC/GR, such as It have been proved that some cells can be induced by stress, and play an important role in stress protein in cell stress, such as heat shock protein 70, can also be induced by GC/GR. The small G protein RhoB is a new GC/GR in recent years, we found that the induced protein. Recent studies abroad show that RhoB is an early response genes can be a variety of genotoxic stress (original induced DNA damage), such as radiation, ultraviolet radiation, anti-cancer drugs (such as 5- fluorouracil, cisplatin) or induced the activation of RhoB has been reported to increase and promote cell survival. But non genotoxic stress also affect the expression of RhoB is not very clear considering RhoB is GR regulatory protein, therefore speculated that this protein may also play a role in non genotoxic stress, the effects of heat stress and hypoxia of the two kinds of non genotoxic stress on the expression of RhoB in vivo and in vitro from two levels, We further studied the mechanism of heat stress affecting the expression of RhoB and its possible biological significance, in order to provide new targets for the treatment of clinical burn and shock.
The inducement, mechanism and biological significance of heat stress on RhoB expression
(1) heat stress can induce the expression of RhoB
We first made scald rat model of 30% body surface area were prepared by semi quantitative RT-PCR, Real-time PCR and Western blot method to detect the expression of mRNA protein and RhoB in liver and lung tissues of rats. The results showed that rat liver and lung tissue in RhoB mRNA in 2h after scald is raised to the maximum value of 4h, the control group respectively 7.5 and 5.7 times (P < 0.01); RhoB protein in rats after the expression of 8h was highest.
Because the body will produce a series of neuroendocrine responses after scald, and our previous experiments also confirmed the expression of GC can induce RhoB. Effects of neuroendocrine factors from the body, to determine whether the heat stress itself can be directly up-regulated RhoB, we further examined the effects of heat stress on the expression of RhoB in cultured cells. And the whole experiment to the liver, lung tissue as the research object corresponding to human hepatoma HepG2 cells and lung adenocarcinoma A549 cells were selected in vitro; considering the liver and lung tissues in addition to parenchymal cells, but also contains a large number of tissue macrophages, so we also selected a mouse macrophage cell line RAW264.7 as the research object. The results showed that heat stress itself in a time-dependent manner rapidly induced by these three kinds of in vitro expression of RhoBmRNA and protein in the cell. The experimental results show that the heat The expression of RhoB can be up-regulated in both in vivo and in vitro, and there is no obvious tissue cell specificity in this induction.
(two) study on the mechanism of heat stress induced RhoB expression
1. the expression of RhoB mRNA up regulated by heat stress is related to the enhancement of its stability
We used actinomycin D (5 g/ml) transcription suppressor gene, to observe the effect of heat stress on the stability of RhoBmRNA, the expression of RhoB induced by heat stress is clear at the transcription level, or at the post transcriptional level. The results showed that heat stress in A549 cells can make the half-life of RhoB by 3.95h increased to 7.1h (P < 0.01), RhoB in RAW264.7 cells the half-life increases from 3.98h to 7.6h (P < 0.01), showed that the expression of RhoB mRNA induced by heat stress mainly by the stability of RhoB increased.
2. the p38 MAPK pathway activated by stress participates in the induction of heat stress on RhoB.
It has been confirmed that p38 MAPK signaling pathway can be a variety of stress including heat stress, the original activation, we observed the effect of p38 MAPK inhibitor SB203580 induced expression of RhoB in heat stress. The results showed that SB203580 culture solution was added to A549 cells in p38 (10 M) inhibited the activation of MAPK, then the cells were heat stress, induced level of RhoB than the untreated SB203580 cells was reduced by 40% (P < 0.01); the level of RhoB induced in RAW264.7 cells was decreased by about 50% (P < 0.01), p38 showed that the activation of MAPK pathway involved in the induction of heat stress on RhoB.
(three) the biological significance and possible mechanism of heat stress induced RhoB expression
1.RhoB up regulation can inhibit the apoptosis induced by heat stress
Although the stress is a defensive reaction, but severe stress can lead to apoptosis. Therefore, we observed the changes of expression of RhoB effect on apoptosis of A549 cells, the biological significance of RhoB increase of heat stress. The results showed that the transfection of wild-type RhoB plasmid RhoB expression, apoptosis rate induced by heat stress 64.1% to 49.5% (P < 0.01), the activation of Caspase3 also decreased significantly; while using RNA interference to reduce the expression of RhoB after activation of heat stress induced apoptosis and the ratio of Caspase3 increased obviously, similar results are also obtained in RAW264.7 cells showed that the upregulation of RhoB can inhibit apoptosis induced by heat stress.
2.RhoB up-regulated the possible mechanism of inhibiting apoptosis induced by heat stress
(1) up regulation of RhoB can enhance the transcriptional activation activity of NF- kappa B
It has been proved that many stressors can activate NF- transcription factor kappa B, activation of NF- kappa B by transcriptional regulation of many genes that regulate cell growth, differentiation, immune and inflammatory responses, and play an important role in stress responses, such as the NF- kappa B has been shown in many kinds of cells can lead to apoptosis resistance to various stressors. Therefore, we further examined the effect of RhoB on activation of NF- kappa B transcription activity. The results showed that in A549 cells and RAW264.7 cells, transfected RhoB-wt plasmid that overexpression of RhoB can increase the basal transcription NF- kappa B activation activity, can also be the transcription of NF- kappa B activation activity increased during heat stress; and the inhibition of RhoB expression by RNA interference method, transcription is inhibited NF- kappa B activation activity. Suggest that upregulation of RhoB may enhance the transcription of NF- kappa B activation play anti apoptotic effect.
(2) the up-regulation of RhoB did not affect the expression of heat shock protein 70 (HSPT0) during heat stress
HSP70 is a nonspecific cell protect protein by heat and other stressors induce, can enhance tolerance to stress, improve the survival rate of cells. Many studies showed that HSP70 of radiation (such as gamma rays), TNF- alpha and other stimulation induced apoptosis is inhibited. Therefore, we also observed the effect of RhoB expression on the expression of HSP70 were found in a study of A549 cells and RAW264.7 cells, whether overexpression of RhoB or by RNA interference method to make the inhibition of the expression, did not affect the expression of HSP70 showed that the inhibitory effect of HSP70 was not involved in RhoB on apoptosis induced by heat stress.
Two, the induction of hypoxia on the expression of RhoB
We first copy the rat model of acute hypoxic hypoxia cabin SD rats in the mixed gas containing 8%O_2,92%N_2 in the detection of the expression of RhoBmRNA and protein in spleen and lung tissue in rats with Real-time PCR and Western blot method. The results showed that hypoxia can be time dependent manner to induce rat spleen, the expression of RhoB mRNA and protein in the lung tissue. Then, we also observed the effect of hypoxia on the expression of RhoB RAW264.7 cells in cultured human lung adenocarcinoma A549 cells and mouse macrophage cell line. The results showed that the expression of hypoxia itself in a time dependent manner by two kinds of cells in RhoB mRNA and protein. The above results this indicates that hypoxia non genotoxic stress is able to induce RhoB expression in vivo and in vitro, no specific tissues and cells and this effect.
To sum up, for the first time found that the experimental heat stress, hypoxia of the two non genotoxic stress were able to induce RhoB expression in the overall level and cell level, and the inducible no obvious tissue and cell specificity. The expression stability of heat stress induced by RhoB and RhoB mRNA mainly is higher, while the heat the stress of p38 MAPK activation is involved in the upregulation of.RhoB RhoB expression upregulation can inhibit apoptosis induced by heat stress, the mechanism is not mediated by HSP70 and RhoB, which may enhance transcription of NF- kappa B activation activity related to this topic. The results suggest that RhoB has the character of cell stress proteins.

【學(xué)位授予單位】：第二軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2008
【分類號(hào)】：R363

【相似文獻(xiàn)】

相關(guān)期刊論文 前10條

1 陳育芬;;磺胺嘧啶鋅過敏1例報(bào)告[J];蛇志;2011年02期

2 彭旦明;劉雯;;燒(燙)傷動(dòng)物模型的建立及評(píng)價(jià)[J];遼寧中醫(yī)雜志;2011年09期

3 吳敏;閔文華;王德偉;;低熱致深度燙傷50例治療分析[J];江蘇醫(yī)藥;2011年15期

4 孫齊英;;殼聚糖對(duì)夏季奶牛血液生化指標(biāo)的影響[J];江漢大學(xué)學(xué)報(bào)(自然科學(xué)版);2011年02期

5 李穎;范蔚林;郭力;;燙傷對(duì)大鼠結(jié)腸Kit、Kitl及Gja1基因表達(dá)與胃腸動(dòng)力的影響[J];瀘州醫(yī)學(xué)院學(xué)報(bào);2011年03期

6 侯小玲;趙連友;陳韻岱;;血管緊張素轉(zhuǎn)化酶抑制劑和抗氧化劑對(duì)濕熱應(yīng)激性大鼠心肌AngⅡ和p22phox表達(dá)的影響[J];心臟雜志;2011年03期

7 韓焱福;孫天駿;;缺氧誘導(dǎo)因子-1α基因在嚴(yán)重燙傷延遲復(fù)蘇大鼠肺組織中的表達(dá)[J];中華損傷與修復(fù)雜志(電子版);2011年01期

8 甘冬雪;古月;郭麗怡;秦錦明;王江元;王宇飛;張宏飛;高俊濤;;替普瑞酮對(duì)中暑大鼠的保護(hù)作用[J];吉林醫(yī)藥學(xué)院學(xué)報(bào);2011年04期

9 ;新型棉布讓你不怕開水燙[J];鄉(xiāng)村科技;2010年09期

10 沈君;;家庭急救 幫孩子度過生死三分鐘[J];愛情婚姻家庭(生活紀(jì)實(shí));2011年09期

相關(guān)會(huì)議論文 前10條

1 余冰;張克英;陳代文;;AMPK在仔豬體內(nèi)的分布及熱應(yīng)激對(duì)AMPK活性的影響[A];中國畜牧獸醫(yī)學(xué)會(huì)動(dòng)物營(yíng)養(yǎng)學(xué)分會(huì)——第九屆學(xué)術(shù)研討會(huì)論文集[C];2004年

2 張錦輝;李中文;賈志君;胡茂穎;林新;陳忠;;產(chǎn)前熱應(yīng)激對(duì)仔鼠生殖腺GABA受體發(fā)育的影響[A];畜牧業(yè)環(huán)境、生態(tài)、安全生產(chǎn)與管理——2010年家畜環(huán)境與生態(tài)學(xué)術(shù)研討會(huì)論文集[C];2010年

3 徐向東;程興仁;滕金山;;熱應(yīng)激與個(gè)人防護(hù)[A];第二屆全國人—機(jī)—環(huán)境系統(tǒng)工程學(xué)術(shù)會(huì)議論文集[C];1995年

4 尹小平;袁慧;張明;;奶牛熱應(yīng)激及對(duì)免疫影響的研究進(jìn)展[A];2003全國家畜內(nèi)科學(xué)學(xué)術(shù)研討會(huì)論文專輯[C];2003年

5 褚耀誠;劉鳳華;許劍琴;;清涼沖劑對(duì)不同環(huán)境溫度下豬血清中NO含量的影響[A];第一屆中國養(yǎng)豬生產(chǎn)和疾病控制技術(shù)大會(huì)——2005中國畜牧獸醫(yī)學(xué)會(huì)學(xué)術(shù)年會(huì)論文集[C];2005年

6 張凡建;王金秋;岳圓;侯引緒;王九峰;;日糧添加有機(jī)鉻對(duì)中度熱應(yīng)激奶牛生理生化指標(biāo)的影響研究[A];中國畜牧獸醫(yī)學(xué)會(huì)家畜內(nèi)科學(xué)分會(huì)第七屆代表大會(huì)暨學(xué)術(shù)研討會(huì)論文集（下冊(cè)）[C];2011年

7 張書霞;華榮虹;鮑恩東;;熱應(yīng)激對(duì)雞免疫器官細(xì)胞凋亡的影響及其調(diào)節(jié)機(jī)理[A];中國畜牧獸醫(yī)學(xué)會(huì)獸醫(yī)病理學(xué)分第12次暨中國動(dòng)物病理生理學(xué)專業(yè)委員會(huì)第11次學(xué)術(shù)討論會(huì)論文集[C];2003年

8 王勝林;方智;;豬的熱應(yīng)激及營(yíng)養(yǎng)調(diào)控的研究進(jìn)展[A];豬營(yíng)養(yǎng)與飼料研究進(jìn)展——第四屆全國豬營(yíng)養(yǎng)學(xué)術(shù)研討會(huì)論文集[C];2003年

9 馮英;田真;高繼偉;曹凱軍;何志清;;奶牛熱應(yīng)激與牛舍的設(shè)計(jì)和建造[A];中國奶業(yè)協(xié)會(huì)年會(huì)論文集2008（上冊(cè)）[C];2008年

10 王建平;;熱應(yīng)激奶牛瘤胃液中溶纖維丁酸弧菌的含量[A];《第六屆中國牛業(yè)發(fā)展大會(huì)》論文集[C];2011年

相關(guān)重要報(bào)紙文章 前10條

1 忱東;夏季家禽熱應(yīng)激病的防治[N];湖北科技報(bào);2000年

2 ;熱應(yīng)激對(duì)養(yǎng)鴿的危害[N];江蘇科技報(bào);2003年

3 長(zhǎng)安區(qū)畜牧獸醫(yī)中心站獸醫(yī)師 每小平;夏季謹(jǐn)防蛋雞熱應(yīng)激[N];陜西科技報(bào);2003年

4 秦發(fā);減少蛋禽熱應(yīng)激技巧[N];陜西科技報(bào);2009年

5 陳芳　李學(xué)俊 劉永恒;夏季如何做好雞的熱應(yīng)激預(yù)防工作[N];中國畜牧獸醫(yī)報(bào);2009年

6 牟定縣畜牧獸醫(yī)局 劉以宏;如何預(yù)防雞熱應(yīng)激[N];云南科技報(bào);2010年

7 安平縣農(nóng)牧局 宋艷敏;夏季如何預(yù)防雞熱應(yīng)激[N];河北科技報(bào);2011年

8 唐山市豐潤(rùn)區(qū)畜牧水產(chǎn)局 李永合;防豬熱應(yīng)激[N];河北科技報(bào);2004年

9 李巧云;可減輕雞熱應(yīng)激的飼料添加劑[N];山東科技報(bào);2005年

10 張邦安;夏季減少蛋禽熱應(yīng)激9竅門[N];中國畜牧獸醫(yī)報(bào);2009年

相關(guān)博士學(xué)位論文 前10條

1 王立志;熱應(yīng)激對(duì)奶牛、奶山羊體內(nèi)內(nèi)毒素含量的影響及緩解熱應(yīng)激的營(yíng)養(yǎng)技術(shù)研究[D];四川農(nóng)業(yè)大學(xué);2010年

2 李憶東;非基因毒應(yīng)激對(duì)小G蛋白R(shí)hoB表達(dá)的誘導(dǎo)作用、機(jī)制及生物學(xué)意義[D];第二軍醫(yī)大學(xué);2008年

3 韓愛云;熱應(yīng)激對(duì)肉雞淋巴細(xì)胞鈣信號(hào)轉(zhuǎn)導(dǎo)的影響及鉻的調(diào)控作用[D];中國農(nóng)業(yè)科學(xué)院;2010年

4 李守軍;肉雞急性熱應(yīng)激損傷及其機(jī)理的研究[D];中國農(nóng)業(yè)大學(xué);2005年

5 李靜;37℃持續(xù)熱應(yīng)激對(duì)肉雞血流動(dòng)力學(xué)和酸堿平衡的影響[D];中國農(nóng)業(yè)大學(xué);2004年

6 張大江;經(jīng)導(dǎo)管肝動(dòng)脈熱碘油栓塞治療原發(fā)性肝癌機(jī)理研究[D];復(fù)旦大學(xué);2003年

7 杜立銀;熱應(yīng)激對(duì)小鼠附植前早期胚胎發(fā)育影響的研究[D];東北農(nóng)業(yè)大學(xué);2005年

8 李守軍;熱休克對(duì)牛卵母細(xì)胞和IVP胚胎影響的研究[D];東北農(nóng)業(yè)大學(xué);2001年

9 朱家橋;DNA甲基化在多囊卵巢綜合征和熱應(yīng)激中的變化及作用[D];甘肅農(nóng)業(yè)大學(xué);2008年

10 胡長(zhǎng)平;辣椒素受體介導(dǎo)吳茱萸次堿的降壓和心臟保護(hù)作用[D];中南大學(xué);2003年

相關(guān)碩士學(xué)位論文 前10條

1 李峰;熱應(yīng)激對(duì)軸索損傷保護(hù)機(jī)制的實(shí)驗(yàn)研究[D];重慶醫(yī)科大學(xué);2004年

2 龔遠(yuǎn)英;肉雞急性熱應(yīng)激損傷與應(yīng)激損傷機(jī)理的研究[D];南京農(nóng)業(yè)大學(xué);2001年

3 付旭彬;肉雞急性熱應(yīng)激損傷及其機(jī)理的研究[D];南京農(nóng)業(yè)大學(xué);2002年

4 孫永建;熱應(yīng)激預(yù)適應(yīng)后HSP70的表達(dá)及其對(duì)大鼠肢體缺血再灌注損傷的影響[D];第一軍醫(yī)大學(xué);2002年

5 張根軍;生長(zhǎng)豬熱應(yīng)激反應(yīng)模型及適宜監(jiān)測(cè)指標(biāo)篩選[D];中國農(nóng)業(yè)科學(xué)院;2004年

6 羅曉鳳;熱應(yīng)激對(duì)血管內(nèi)皮細(xì)胞增殖的影響及CASK增殖信號(hào)通路的研究[D];第三軍醫(yī)大學(xué);2002年

7 蔣定文;胸腺基質(zhì)細(xì)胞對(duì)熱應(yīng)激小鼠胸腺細(xì)胞調(diào)節(jié)作用的研究[D];第一軍醫(yī)大學(xué);2000年

8 白兆鵬;硫辛酸對(duì)熱應(yīng)激下產(chǎn)蛋雞生產(chǎn)性能及抗氧化能力的研究[D];東北農(nóng)業(yè)大學(xué);2004年

9 李俊杰;熱應(yīng)激對(duì)種公牛精液品質(zhì)的影響及機(jī)理研究[D];河北農(nóng)業(yè)大學(xué);2001年

10 李東紅;熱應(yīng)激對(duì)肉雞實(shí)驗(yàn)性大腸桿菌病發(fā)病過程的影響[D];中國農(nóng)業(yè)大學(xué);2005年

，

本文編號(hào)：1356073