本文選題：NG2蛋白多糖 + 腎小球系膜細(xì)胞��； 參考：《華中科技大學(xué)》2012年博士論文

【摘要】：第一部分NG2蛋白多糖在腎小球中的表達(dá)及定位 目的：觀察大鼠乳鼠腎組織中NG2蛋白多糖的表達(dá)及其在腎小球的定位,對(duì)三種腎小球固有細(xì)胞系進(jìn)行檢測(cè),明確NG2在腎小球三種固有細(xì)胞中的具體表達(dá)情況。 方法：選擇出生1天的Wistar大鼠乳鼠,將其腎組織進(jìn)行固定、包埋后制成石蠟切片,免疫組化檢測(cè)觀察NG2在大鼠乳鼠腎組織的分布,對(duì)腎小球中NG2的表達(dá)進(jìn)行定位。以RPMI1640培養(yǎng)基培養(yǎng)條件永生化小鼠足細(xì)胞,DMEM培養(yǎng)基培養(yǎng)大鼠系膜細(xì)胞,DMEM/F12培養(yǎng)基培養(yǎng)小鼠內(nèi)皮細(xì)胞。間接免疫熒光染色共聚焦顯微鏡下觀察三種腎小球固有細(xì)胞中NG2蛋白的表達(dá)情況。以RT-PCR法檢測(cè)足細(xì)胞、系膜細(xì)胞和內(nèi)皮細(xì)胞中NG2mRNA的表達(dá)。 結(jié)果：NG2蛋白在腎組織中有陽(yáng)性表達(dá),在腎小球中主要定位于系膜細(xì)胞及其周圍系膜區(qū)。在系膜細(xì)胞中NG2蛋白呈陽(yáng)性表達(dá),NG2均勻分布在系膜細(xì)胞胞膜上,而在細(xì)胞核上無(wú)表達(dá)；NG2蛋白在足細(xì)胞和內(nèi)皮細(xì)胞中均無(wú)陽(yáng)性表達(dá)。RT-PCR從mRNA水平證實(shí)了在三種腎小球固有細(xì)胞中,NG2僅在系膜細(xì)胞中表達(dá)。 結(jié)論：腎小球中NG2表達(dá)于間葉組織來(lái)源的腎小球系膜細(xì)胞,在系膜細(xì)胞及其周圍的系膜區(qū)均有表達(dá),而在另外兩種腎小球固有細(xì)胞中無(wú)表達(dá),提示腎小球中NG2由系膜細(xì)胞分泌,并向周圍系膜基質(zhì)中釋放。第二部分LPS刺激后大鼠腎小球中NG2蛋白多糖和炎癥因子的表達(dá)變化 目的：觀察脂多糖(LPS)刺激后大鼠乳鼠腎小球中NG2蛋白多糖的表達(dá)及促 炎因子腫瘤壞死因子-a(TNF-aa)和白細(xì)胞介素-1p(IL-1β)的表達(dá)變化,初步 探討NG2與腎小球炎癥反應(yīng)之間的關(guān)系。 方法：選擇出生1天的Wistar大鼠乳鼠30只,分為3組：對(duì)照組、LPS組和LPS+Dex組,分別腹腔注射生理鹽水、LPS和LPS+Dexamethasone。12小時(shí)后,取其一側(cè)腎組織進(jìn)行固定、包埋后制成石蠟切片,免疫組化檢測(cè)NG2在腎小球中的表達(dá)變化。另一側(cè)腎組織篩網(wǎng)法分離腎小球,提取腎小球mRNA和蛋白質(zhì),實(shí)時(shí)熒光定量PCR檢測(cè)NG2、TNF-aa和IL-1βmRNA的表達(dá),ELISA檢測(cè)腎小球中NG2、TNF-a和IL-1β蛋白的表達(dá)。 結(jié)果：NG2免疫組化結(jié)果顯示,NG2蛋白在腎小球系膜細(xì)胞及周圍基質(zhì)中表達(dá),與對(duì)照組相比,LPS刺激后NG2蛋白表達(dá)明顯增多；LPS刺激并與Dexamethasone干預(yù)后NG2蛋白表達(dá)較LPS組減少。分離的腎小球提取RNA,實(shí)時(shí)熒光定量PCR結(jié)果顯示,LPS刺激后腎小球中NG2、TNF-a和IL-1β mRNA相對(duì)表達(dá)水平均高于對(duì)照組,差異有統(tǒng)計(jì)學(xué)意義(P0.01)；LPS刺激并與Dexamethasone干預(yù)后腎小球中NG2、TNF-a和IL-1β mRNA相對(duì)表達(dá)水平均較LPS組降低,差異有統(tǒng)計(jì)學(xué)意義(P0.01)。分離的腎小球提取蛋白,ELISA結(jié)果顯示,與對(duì)照組相比,LPS刺激后RMC中NG2、TNF-a和IL-1p蛋白表達(dá)水平均升高,差異有統(tǒng)計(jì)學(xué)意義(P0.01)；LPS刺激并與Dexamethasone干預(yù)后RMC中NG2、TNF-a和IL-1p蛋白表達(dá)水平較LPS組均降低,差異有統(tǒng)計(jì)學(xué)意義(P0.01)。 結(jié)論：腎小球系膜細(xì)胞NG2高表達(dá)與腎小球炎癥密切相關(guān),NG2可誘導(dǎo)促炎因子TNF-a和IL-1p高表達(dá),通過(guò)TNF-a和IL-1β介導(dǎo)腎小球炎癥反應(yīng)。介素-1p 第三部分NG2蛋白多糖在腎小球炎癥與系膜細(xì)胞增殖中的作用 目的：觀察LPS刺激后NG2蛋白多糖和促炎因子TNF-a和IL-1p在大鼠系膜細(xì)胞(RMC)的表達(dá)變化,以及RMC的增殖情況；NG2-siRNA轉(zhuǎn)染RMC下調(diào)NG2表達(dá)后,觀察促炎因子TNF-a和IL-1p的表達(dá)變化及RMC增殖的變化,探討NG2與腎小球炎癥反應(yīng)及系膜細(xì)胞增殖之間的關(guān)系。 方法：(1)體外培養(yǎng)RMC,將細(xì)胞分為3組：對(duì)照組、LPS組和LPS+Dex組,干預(yù)8小時(shí)后,間接免疫熒光染色觀察NG2蛋白的表達(dá),實(shí)時(shí)熒光定量PCR檢測(cè)RMC中NG2、TNF-a和IL-1β mRNA的表達(dá),ElISA檢測(cè)RMC培養(yǎng)上清液中NG2、TNF-a和IL-1p,MTT檢測(cè)RMC增殖情況。(2)設(shè)計(jì)及合成NG2-siRNA,用脂質(zhì)體法將其轉(zhuǎn)入體外培養(yǎng)的RMC,24小時(shí)后熒光顯微鏡下觀察轉(zhuǎn)染標(biāo)志Cy3的表達(dá)；48小時(shí)后PCR檢測(cè)NG2的干擾效率。(3)將細(xì)胞分為3組：正常對(duì)照組、LPS干預(yù)組和LPS干預(yù)+轉(zhuǎn)染NG2-siRNA組。NG2-siRNA轉(zhuǎn)染及LPS干預(yù)8小時(shí)后,實(shí)時(shí)熒光定量PCR檢測(cè)RMC中NG2、TNF-a和IL-1βmRNA的表達(dá),ElISA檢測(cè)RMC培養(yǎng)上清液中NG2、TNF-a和IL-1β,MTT檢測(cè)RMC增殖情況。 結(jié)果：(1)LPS刺激RMC8小時(shí)后免疫熒光結(jié)果顯示,與對(duì)照組相比LPS組中NG2蛋白表達(dá)明顯增多,且分布均勻。LPS+Dex組NG2蛋白表達(dá)較LPS組減少,但仍多于對(duì)照組。(2)實(shí)時(shí)熒光定量PCR和ELISA結(jié)果顯示,LPS刺激8小時(shí)后RMC中NG2、TNF-α、IL-1β mRNA和RMC培養(yǎng)上清液中NG2、TNF-a、IL-1p蛋白表達(dá)水平均升高,RMC增殖效率上升,與對(duì)照組相比,差異均有統(tǒng)計(jì)學(xué)意義(P0.01)。Dexamethasone干預(yù)可部分逆轉(zhuǎn)上述反應(yīng)。(3)NG2-siRNA轉(zhuǎn)染24小時(shí)后,Cy3呈強(qiáng)熒光表達(dá)；實(shí)時(shí)熒光定量PCR結(jié)果顯示,與未轉(zhuǎn)染對(duì)照組及陰性siRNA轉(zhuǎn)染組相比,NG2-siRNA轉(zhuǎn)染組NG2表達(dá)顯著下降,達(dá)到下調(diào)NG2表達(dá)的效果。(4)LPS刺激RMC8小時(shí)后,與對(duì)照組相比,RMC中NG2、TNF-α、IL-1β mRNA和RMC培養(yǎng)上清液中NG2、TNF-a、IL-1β蛋白表達(dá)水平均升高, RMC增殖效率上升,而NG2-siRNA可逆轉(zhuǎn)上述反應(yīng),差異有統(tǒng)計(jì)學(xué)意義(P0.01)。 結(jié)論：體外LPS刺激RMC后可NG2表達(dá)增加,促炎因子TNF-a和IL-1β的釋放增加,RMC增殖效率上升,NG2基因沉默可逆轉(zhuǎn)上述反應(yīng)。因此,NG2介導(dǎo)促炎因子TNF-a和IL-1β等的釋放,且通過(guò)腎小球炎癥反應(yīng)的激活促進(jìn)系膜細(xì)胞增殖。
[Abstract]:The first part is the expression and localization of NG2 proteoglycan in the glomerulus.
Objective: To observe the expression of NG2 proteoglycan in the renal tissue of rats and the location of the glomeruli, to detect the three kinds of glomerular innate cell lines and to clarify the specific expression of NG2 in the three kinds of glomerular mesangial cells.
Methods: the Wistar rats of 1 days of birth were selected to fix the renal tissue and be embedded into paraffin section. The distribution of NG2 in the renal tissue of rats was detected by immunohistochemistry and the expression of NG2 in the glomeruli was located. The rat mesangial cells were immortalized by the culture condition of RPMI1640 medium, and the mesangial cells were cultured in the DMEM medium. Mouse endothelial cells were cultured on DMEM/F12 medium. The expression of NG2 protein in three glomerular innate cells was observed under indirect immunofluorescence staining microscope. The expression of NG2mRNA in podocytes, mesangial cells and endothelial cells was detected by RT-PCR.
Results: the positive expression of NG2 protein in the renal tissue is mainly located in the mesangial cells and the surrounding mesangial region. In the mesangial cells, the NG2 protein is positive, and the NG2 is distributed evenly on the membrane of the mesangial cells, but no expression in the nucleus, and the NG2 protein has no positive expression of.RT-PCR from mRNA in the podocytes and endothelial cells. It is confirmed that NG2 is only expressed in mesangial cells in three types of glomerular intrinsic cells.
Conclusion: NG2 expressed in mesangial mesangial cells derived from mesangial cells and the mesangial region around mesangial cells, but not expressed in the other two kinds of glomerular innate cells, suggesting that the glomerular NG2 is secreted by mesangial cells and released into the peripheral mesangial matrix. The second part of LPS stimulates the rat glomeruli. Expression of NG2 proteoglycan and inflammatory factors
Objective: To observe the expression and promotion of NG2 proteoglycan in glomeruli of rats after lipopolysaccharide (LPS) stimulation.
Expression of inflammatory factors, tumor necrosis factor -a (TNF-aa) and interleukin -1p (IL-1 beta), were preliminarily studied.
To investigate the relationship between NG2 and glomerular inflammatory response.
Methods: 30 Wistar rats were selected for 1 days of birth. They were divided into 3 groups: control group, LPS group and LPS+Dex group. After intraperitoneal injection of saline, LPS and LPS+Dexamethasone.12 hours, the kidney tissue was fixed and embedded into paraffin section. The expression of NG2 in the glomeruli was detected by immunohistochemistry. The other side of renal tissue was screened. Glomeruli was separated by net method. Glomerular mRNA and protein were extracted. The expression of NG2, TNF-aa and IL-1 beta mRNA were detected by real-time fluorescence quantitative PCR. The expression of NG2, TNF-a and IL-1 beta in glomeruli was detected by ELISA.
Results: the results of NG2 immunohistochemical staining showed that NG2 protein was expressed in mesangial cells and surrounding matrix. Compared with the control group, the expression of NG2 protein increased significantly after LPS stimulation. LPS stimulated and NG2 protein expression decreased after Dexamethasone intervention. The isolated glomeruli extracted RNA, real-time fluorescent quantitative PCR results showed, LPS stimulation after stimulation. The relative expression level of NG2, TNF-a and IL-1 beta mRNA in the glomeruli was higher than that in the control group (P0.01). LPS stimulation and the relative expression level of TNF-a and IL-1 beta mRNA after Dexamethasone intervention were lower than that of LPS group. Compared with the control group, the expression level of NG2, TNF-a and IL-1p protein in RMC increased after LPS stimulation, and the difference was statistically significant (P0.01). LPS stimulation and NG2, TNF-a and IL-1p protein expression levels in RMC decreased after the intervention of Dexamethasone, and the difference was statistically significant.
Conclusion: the high expression of NG2 in mesangial mesangial cells is closely related to glomerular inflammation. NG2 can induce the high expression of TNF-a and IL-1p, and mediate the glomerular inflammatory reaction through TNF-a and IL-1 beta. The mediator -1p is mediated.
The third part is the role of NG2 proteoglycan in glomerulonephritis and mesangial cell proliferation.
Objective: To observe the expression of NG2 proteoglycan and proinflammatory factor TNF-a and IL-1p in rat mesangial cells (RMC) and the proliferation of RMC after LPS stimulation. After NG2-siRNA transfected with RMC, the expression of TNF-a and IL-1p and the proliferation of RMC were observed and the proliferation of glomerular inflammation and mesangial cells were observed. The relationship between them.
Methods: (1) the RMC was cultured in vitro, and the cells were divided into 3 groups: the control group, the LPS group and the LPS+Dex group. After 8 hours of intervention, the expression of NG2 protein was observed by indirect immunofluorescence staining. The expression of NG2, TNF-a and IL-1 beta mRNA in RMC was detected by real-time fluorescent quantitative PCR, and the proliferation of RMC culture supernatant was detected by ElISA detection. (2) design and NG2-siRNA was synthesized with liposome method and transferred into RMC in vitro. After 24 hours, the expression of transfection marker Cy3 was observed. The interference efficiency of NG2 was detected by PCR after 48 hours. (3) the cells were divided into 3 groups: normal control group, LPS intervention group and LPS intervention + transfected NG2-siRNA group.NG2-siRNA transfection and LPS intervention for 8 hours, real time fluorescence Quantitative PCR was used to detect the expression of NG2, TNF-a and IL-1 beta mRNA in RMC. ElISA was used to detect NG2, TNF-a and IL-1 beta in RMC culture supernatant, and the proliferation was detected by TNF-a.
Results: (1) the immunofluorescence results of LPS stimulation after RMC8 hours showed that the expression of NG2 protein in the LPS group was significantly increased compared with the control group, and the NG2 protein expression in the.LPS+Dex group was less than that in the LPS group, but it was still more than the control group. (2) the real-time fluorescence quantitative PCR and ELISA results showed that LPS stimulated 8 hours after the RMC NG2. The expression level of NG2, TNF-a, IL-1p protein in the supernatant increased and the proliferation efficiency of RMC increased. Compared with the control group, the difference was statistically significant (P0.01).Dexamethasone intervention could partly reverse the above reaction. (3) Cy3 showed strong fluorescent expression after 24 hours of NG2-siRNA transfection, and the real time fluorescence quantitative PCR results showed that the control group and negative siR were not transfected with the control group and negative siR. Compared with the NA transfection group, the expression of NG2 decreased significantly in the NG2-siRNA transfection group. (4) after LPS stimulation for RMC8 hours, the expression level of NG2, TNF- alpha, IL-1 beta and RMC culture supernatant in RMC was higher than that of the control group, and the expression level of the beta protein increased and the proliferation efficiency increased. Study meaning (P0.01).
Conclusion: after LPS stimulation of RMC in vitro, the expression of NG2 increased, the release of pro-inflammatory factor TNF-a and IL-1 beta was increased, the proliferation efficiency of RMC increased, and NG2 gene silencing could reverse the above reaction. Therefore, NG2 mediated the release of TNF-a and IL-1 beta, and promoted the proliferation of mesangial cells through the activation of glomerular inflammatory reaction.
【學(xué)位授予單位】：華中科技大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2012
【分類號(hào)】：R363

【相似文獻(xiàn)】

相關(guān)期刊論文 前10條

1 曾祥元,顧大勇,馬布仁,陳莉,楊季云,王天然,唐旭東,石力;LPS誘導(dǎo)肺微血管內(nèi)皮細(xì)胞與PMN的粘附作用及核調(diào)控機(jī)理的實(shí)驗(yàn)研究[J];中國(guó)微循環(huán);2002年05期

2 羅向東,石富勝,王曉軍,楊宗誠(chéng),黎鰲;LPS對(duì)血管內(nèi)皮細(xì)胞的直接損傷作用的初步研究[J];第三軍醫(yī)大學(xué)學(xué)報(bào);2003年18期

3 劉小麗 ,顧大勇 ,馬布仁 ,陳莉 ,曾祥元 ,唐旭東 ,許瑋;LPS直接誘導(dǎo)的肺微血管內(nèi)皮細(xì)胞與PMN的粘附作用及核因子κB調(diào)控機(jī)理的實(shí)驗(yàn)研究[J];青海醫(yī)藥雜志;2003年01期

4 王梁華,朱玉平,潘衛(wèi),婁永華,陳建鶴,馮煜,焦炳華;LPS、rh-TNFα刺激PBL誘導(dǎo)TRAIL表達(dá)的初步研究[J];免疫學(xué)雜志;1999年03期

5 高明霞,李康生;大蒜對(duì)老齡BALB/c小鼠血漿IL-1β、IL-6水平影響的研究[J];上海免疫學(xué)雜志;2000年06期

6 顧大勇,曾祥元,陳莉,楊季云,馬布仁,王天然,唐旭東,石力;LPS誘導(dǎo)肺微血管內(nèi)皮細(xì)胞ICAM-1的表達(dá)及NF-κB作用的實(shí)驗(yàn)研究[J];中國(guó)微循環(huán);2002年01期

7 孫可一,季曉輝,馮艷紅,殷國(guó)慶;內(nèi)毒素休克獼猴白細(xì)胞介素18 mRNA變化規(guī)律的研究[J];中國(guó)免疫學(xué)雜志;2004年03期

8 李凡,石艷春,李中秋,陳立,盧丹,姜秀英,陳玉全;臭冷杉精油對(duì)小鼠T、B淋巴細(xì)胞增殖反應(yīng)的影響[J];吉林中醫(yī)藥;1998年02期

9 楊志軍,葛煦,饒志仁,段麗,鞠躬;Fos蛋白在LPS免疫激發(fā)大鼠腦內(nèi)的分布[J];解剖學(xué)報(bào);2000年04期

10 李凌波,朱孔黎,楊渝珍,龔非力;LPS刺激對(duì)TACE基因表達(dá)和對(duì)TNF-α前體加工的影響[J];中國(guó)免疫學(xué)雜志;2002年10期

相關(guān)會(huì)議論文 前10條

1 何文喜;Cooper PR;Anthony J.Smith;;LPS對(duì)牙本質(zhì)涎磷蛋白基因表達(dá)調(diào)控的研究[A];全國(guó)第三次牙體牙髓病學(xué)臨床技術(shù)研討會(huì)論文匯編[C];2009年

2 翟維佳;;LPS對(duì)宮頸癌細(xì)胞HMGB1主動(dòng)釋放的影響[A];中國(guó)抗癌協(xié)會(huì)婦科腫瘤專業(yè)委員會(huì)第十一屆全國(guó)學(xué)術(shù)會(huì)議論文匯編[C];2011年

3 何文喜;余擎;吳張萍;張菁;Anthony J.Smith;;LPS對(duì)成牙本質(zhì)細(xì)胞內(nèi)DCN基因表達(dá)的影響[A];全國(guó)第八次牙體牙髓病學(xué)學(xué)術(shù)會(huì)議論文匯編[C];2011年

4 陳旭林;郭峰;王飛;王永杰;;不同濃度的LPS對(duì)RAW264.7巨噬細(xì)胞血管緊張素Ⅱ1型受體表達(dá)的影響[A];中華醫(yī)學(xué)會(huì)燒傷外科學(xué)分會(huì)2009年學(xué)術(shù)年會(huì)論文匯編[C];2009年

5 翟維佳;蔡紅兵;李偉;;LPS對(duì)Hela細(xì)胞HMGB1主動(dòng)釋放的影響[A];中國(guó)抗癌協(xié)會(huì)婦科腫瘤專業(yè)委員會(huì)第十一屆全國(guó)學(xué)術(shù)會(huì)議論文匯編[C];2011年

6 胡靜;王宏健;申曉輝;何曉凡;賀石林;文志斌;;血管緊張素-(1-7)對(duì)脂多糖誘導(dǎo)血管內(nèi)皮細(xì)胞組織因子表達(dá)的影響及其機(jī)制研究[A];中國(guó)生理學(xué)會(huì)第23屆全國(guó)會(huì)員代表大會(huì)暨生理學(xué)學(xué)術(shù)大會(huì)論文摘要文集[C];2010年

7 段光杰;劉友生;朱江;許成燕;徐小明;;合成的MD-2模擬肽體外抑制LPS誘導(dǎo)的過(guò)度炎癥反應(yīng)[A];中華醫(yī)學(xué)會(huì)病理學(xué)分會(huì)2010年學(xué)術(shù)年會(huì)日程及論文匯編[C];2010年

8 陳翠萍;董思國(guó);;用酶標(biāo)抑制法檢測(cè)霍亂疫苗中LPS含量的研究[A];第五次全國(guó)免疫診斷暨疫苗學(xué)術(shù)研討會(huì)論文匯編[C];2011年

9 羅百靈;張樂(lè)蒙;;LPS誘導(dǎo)鼠巨噬細(xì)胞株RAW264.7細(xì)胞IRF-1的表達(dá)及信號(hào)傳導(dǎo)通路研究[A];中華醫(yī)學(xué)會(huì)呼吸病學(xué)年會(huì)——2011（第十二次全國(guó)呼吸病學(xué)學(xué)術(shù)會(huì)議）論文匯編[C];2011年

10 孟愛(ài)宏;;p38MAPK和STAT3在LPS刺激小鼠肺泡巨噬細(xì)胞中的作用[A];中國(guó)病理生理學(xué)會(huì)第九屆全國(guó)代表大會(huì)及學(xué)術(shù)會(huì)議論文摘要[C];2010年

相關(guān)重要報(bào)紙文章 前5條

1 本報(bào)記者黃志凌;西部利用外資升溫[N];四川日?qǐng)?bào);2002年

2 江東 蘇曄;臺(tái)灣鋁材榕城走俏[N];中國(guó)質(zhì)量報(bào);2000年

3 詹建 宋純東;益氣養(yǎng)陰清熱化瘀 治系膜增生性腎炎[N];健康報(bào);2002年

4 曉符;顯示器市場(chǎng)：群雄逐鹿中原[N];中國(guó)企業(yè)報(bào);2002年

5 南方周末記者 黃永明　南方周末實(shí)習(xí)生 王寅;讓免疫學(xué)進(jìn)入細(xì)胞和分子層面[N];南方周末;2011年

相關(guān)博士學(xué)位論文 前10條

1 史秀巖;NG2蛋白多糖在LPS誘導(dǎo)的腎小球炎癥及系膜細(xì)胞增殖中的作用[D];華中科技大學(xué);2012年

2 趙延濤;LPS致流產(chǎn)作用及保胎中藥的調(diào)控效應(yīng)研究[D];河北農(nóng)業(yè)大學(xué);2011年

3 鄧小鹿;p115RhoGEF/RhoA信號(hào)通路參與調(diào)控LPS及TNF-α致腦微血管內(nèi)皮細(xì)胞通透性增高的機(jī)制研究[D];中南大學(xué);2012年

4 張樂(lè)蒙;IRF-1對(duì)LPS誘導(dǎo)的小鼠巨噬細(xì)胞凋亡和自噬的調(diào)節(jié)作用及其機(jī)制研究[D];中南大學(xué);2012年

5 楊曉萍;1，，25-二羥維生素D3對(duì)大鼠系膜細(xì)胞增殖與凋亡的影響及其機(jī)制探討[D];華中科技大學(xué);2010年

6 許敏;HIF-1α在丹參酮ⅡA減輕內(nèi)毒素性急性肺損傷中的作用及其機(jī)制研究[D];第四軍醫(yī)大學(xué);2011年

7 劉耀;鱟抗內(nèi)毒素因子模擬肽CLP-19抑制LPS的免疫應(yīng)答作用研究[D];第三軍醫(yī)大學(xué);2011年

8 曲忠花;HBV對(duì)補(bǔ)體殺傷作用的影響及LPS對(duì)胞內(nèi)DNA免疫的作用研究[D];山東大學(xué);2010年

9 曲玲;LRP16基因調(diào)控LPS/TLR4信號(hào)通路的作用與機(jī)制研究[D];中國(guó)人民解放軍軍醫(yī)進(jìn)修學(xué)院;2012年

10 田豐;SIGIRR在LPS誘導(dǎo)的人肺泡II型上皮細(xì)胞（A549）急性炎癥反應(yīng)中的作用[D];第四軍醫(yī)大學(xué);2010年

相關(guān)碩士學(xué)位論文 前10條

1 楊倩;槲皮素抗LPS致小鼠胚泡著床障礙作用的研究[D];河北農(nóng)業(yè)大學(xué);2011年

2 刁歡;多不飽和脂肪酸對(duì)LPS誘導(dǎo)的多巴胺能神經(jīng)元損傷的作用及機(jī)理研究[D];第四軍醫(yī)大學(xué);2010年

3 刁歡;多不飽和脂肪酸對(duì)LPS誘導(dǎo)的多巴胺能神經(jīng)元損傷的作用及機(jī)理研究[D];第四軍醫(yī)大學(xué);2010年

4 徐棟花;乳酸桿菌對(duì)LPS誘導(dǎo)THP-1細(xì)胞炎癥性細(xì)胞因子釋放的調(diào)節(jié)作用及可能機(jī)制[D];南京醫(yī)科大學(xué);2011年

5 錢鳳英;MEKK3在LPS刺激后惡性腫瘤細(xì)胞產(chǎn)生IL-6作用中的初步研究[D];福建醫(yī)科大學(xué);2011年

6 鄧華明;蛇床子素對(duì)LPS誘導(dǎo)的小膠質(zhì)細(xì)胞活化的影響[D];暨南大學(xué);2011年

7 李楊;LPS對(duì)羧酸酯酶1和2（CES1、CES2）表達(dá)的研究[D];南京醫(yī)科大學(xué);2010年

8 董莎莎;云芝糖肽（PSP）對(duì)LPS刺激的小鼠巨噬細(xì)胞ROS及MAPK信號(hào)通路的研究[D];上海師范大學(xué);2011年

9 劉靜;乳酸抑制LPS激活大鼠腸黏膜微血管內(nèi)皮細(xì)胞NF-κB通路的研究[D];北京農(nóng)學(xué)院;2011年

10 馮琳琳;LPS、TGF-β1對(duì)小鼠BMDC的影響及TGF-βRⅠ在哮喘遺傳背景不同小鼠BMDC中的研究[D];重慶醫(yī)科大學(xué);2010年

本文編號(hào)：1998655