本文關(guān)鍵詞：肝臟交感神經(jīng)調(diào)控與急性肝損傷關(guān)系的實(shí)驗(yàn)研究　出處：《第三軍醫(yī)大學(xué)》2010年碩士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 肝損傷 去交感神經(jīng) 去甲腎上腺素 四氯化碳 神經(jīng)電生理 腫瘤壞死因子 枯否細(xì)胞 TNF-a和IL-1βmRNA 內(nèi)毒素

【摘要】： 一、背景 在臨床中,由于嚴(yán)重外傷,肝臟大手術(shù)、藥物中毒、細(xì)菌、病毒感染等原因?qū)е碌募毙愿螕p傷容易導(dǎo)致急性肝衰竭。目前對(duì)于急性肝損傷所致的肝功能不全或急性肝功能衰竭,臨床治療十分棘手,藥物保肝難以收到理想的療效。在此病理過程中,由于外傷、細(xì)菌、病毒等直接造成的肝細(xì)胞損害是有限的,而機(jī)體自身對(duì)一些輕微的損害或病原體的不適當(dāng)?shù)难装Y或免疫反應(yīng)可能造成嚴(yán)重的后果。過強(qiáng)的炎癥反應(yīng)使大量炎性介質(zhì)進(jìn)入血循環(huán)可造成全身炎癥反應(yīng)綜合征(systemic inflammatory response syndrome, SIRS)、引起休克和多系統(tǒng)臟器功能衰竭(multi-system/organ failure, MSOF),急性肝損傷是屬于全身炎癥反應(yīng)綜合征的一個(gè)臟器表現(xiàn)。 炎癥的發(fā)生與發(fā)展是一個(gè)復(fù)雜的過程,受到很多因素的影響和調(diào)節(jié)。參與機(jī)體炎癥反應(yīng)的調(diào)控因素可大致分為體液和神經(jīng)兩大類,其中單核巨噬細(xì)胞在炎癥中發(fā)揮極其關(guān)鍵的作用。當(dāng)前有關(guān)炎癥反應(yīng)與肝損傷的研究主要集中在體液調(diào)節(jié)方面,對(duì)于神經(jīng)調(diào)控方面的研究由于缺乏良好的動(dòng)物模型,研究資料較少顯示。肝臟交感神經(jīng)調(diào)控系統(tǒng)由腹腔神經(jīng)節(jié)、脊髓胸腰段、下丘腦交感中樞三個(gè)不同層次的中樞構(gòu)成。肝臟中kupffer細(xì)胞是單核巨噬細(xì)胞系統(tǒng)中的主要成員,是居留在肝臟中的巨噬細(xì)胞,占全身巨噬細(xì)胞總數(shù)的80%以上,占肝臟非實(shí)質(zhì)細(xì)胞數(shù)量的35%,起重要的防御功能。Kupffer細(xì)胞的激活與肝臟急、慢性炎癥關(guān)系密切。 綜合近年來國內(nèi)外的研究結(jié)果,我們推斷在急性肝損傷的發(fā)生、發(fā)展中,隨著交感神經(jīng)活性的改變,交感神經(jīng)系統(tǒng)各級(jí)中樞完全有可能通過對(duì)神經(jīng)遞質(zhì)釋放的調(diào)節(jié)直接調(diào)控Kupffer細(xì)胞表達(dá)炎癥相關(guān)因子,從而參與啟動(dòng)和觸發(fā)了過度炎癥反應(yīng)。 二、目的 本研究擬從肝臟交感神經(jīng)調(diào)控系統(tǒng)的不同節(jié)段去交感處理,探討交感神經(jīng)系統(tǒng)各個(gè)節(jié)段在急性肝損傷中的調(diào)控效能,并通過體外實(shí)驗(yàn)初步驗(yàn)證交感神經(jīng)活化在急性肝損傷發(fā)生、發(fā)展中的調(diào)節(jié)效應(yīng)。以從新的角度重新認(rèn)識(shí)全身炎癥反應(yīng)及相應(yīng)臟器損傷的調(diào)節(jié)機(jī)制,為過度炎癥反應(yīng)(SIRS)以及MODS的治療提供了新的思路。 三、方法與結(jié)果 1、不同節(jié)段去交感神經(jīng)對(duì)CCL4所致大鼠急性肝損傷的影響:從頸交感神經(jīng)干、內(nèi)臟大神經(jīng)以及肝內(nèi)神經(jīng)末稍不同調(diào)控節(jié)段阻斷交感神經(jīng)的傳導(dǎo)通路,在此基礎(chǔ)上應(yīng)用CCL4制作急性肝損傷模型。用記錄電極測定交感神經(jīng)沖動(dòng)的發(fā)放頻率和波幅變化,肝功能、血清TNF-a濃度以及肝組織病理學(xué)、高效液相色譜法測定肝組織內(nèi)NE等有關(guān)指標(biāo)。①正常大鼠頸交感神經(jīng)干放電波幅較低、頻率均一、電壓趨于平穩(wěn),經(jīng)CCL4腹腔內(nèi)注射行肝損傷刺激以后,交感神經(jīng)干放電立刻增加、波伏增大,呈脈沖式增強(qiáng),持續(xù)記錄約40秒鐘后,交感神經(jīng)電活動(dòng)回復(fù)正常時(shí)波形。②頸交感干離段、肝內(nèi)去交感組分別和shame組比較:白蛋白和前白蛋白增高,AST、ALT,總膽紅素等各項(xiàng)肝功能指標(biāo)顯著降低,差異具有顯著性(P0.05, P0.01)。內(nèi)臟大神經(jīng)離斷和shame組比較各項(xiàng)肝功能指標(biāo)差異無顯著性(P0.05)。③頸交感干離斷組和肝內(nèi)去交感分別與shame組比較,肝組織內(nèi)去甲腎上腺素濃度明顯降低,差異非常顯著(P0.01)。內(nèi)臟大神經(jīng)離斷和shame組比較無明顯變化,結(jié)果統(tǒng)計(jì)無差異(P0.05)。④頸交感干離斷、肝內(nèi)去交感組血清TNF-a水平較shame明顯降低(P0.05),內(nèi)臟大神經(jīng)離斷組較shame組升高。 2、交感神經(jīng)遞質(zhì)NE對(duì)內(nèi)毒素誘導(dǎo)大鼠kupffer細(xì)胞TNF-a/ IL-1β表達(dá)的影響采用原位灌注、IV型膠原酶消化、percoll密度梯度離心,選擇性貼壁等方法分離純化得到的kupffer細(xì)胞分為三組培養(yǎng)。A組(空白對(duì)照組);B組(LPS);C組(LPS+NE )分別采用Real time PCR和ELISA檢測KC的TNF-α、IL-1βmRNA和蛋白水平表達(dá)。①KC細(xì)胞正常情況下幾乎不表達(dá)TNF-a和IL-1β,經(jīng)外源性內(nèi)毒素LPS(終濃度為10μg/ml)的刺激后,在12小時(shí)TNF-a、IL-1βmRNA表達(dá)顯著增加;而在加入去甲腎上腺素終濃度為1μmol/L及10μmol/L培養(yǎng)液的處理組中,TNF-a mRNA水平與LPS組比較分別增加50.9% (P0.05)和59.1% (P0.05) ,IL-1βmRNA水平較LPS組增加53.7%(P0.05)和57.8%(P0.05),其表達(dá)量與去甲腎上腺素濃度呈正相關(guān);②TNF-a、IL-1β在蛋白水平和mRNA水平結(jié)果一致。正常情況下幾乎不表達(dá)或微量表達(dá),LPS(10μg/ml)刺激后表達(dá)顯著增高。(LPS+NE)共刺激后,TNF-a、IL-1β濃度在去甲腎上腺素濃度為1μmol/L及10μmol/L時(shí)較LPS組明顯增加(P0.05),而在低濃度(0.1μmol/L)情況下,結(jié)果無顯著差異。 結(jié)論: 1、交感神經(jīng)調(diào)控系統(tǒng)不同節(jié)段去交感神經(jīng),可顯著減輕CCL4所致急性肝損傷時(shí)肝功能損害,肝組織內(nèi)去甲腎上腺素水平隨之降低。交感神經(jīng)系統(tǒng)各個(gè)節(jié)段具有相對(duì)獨(dú)立的調(diào)控功能以調(diào)控維持機(jī)體機(jī)能穩(wěn)定,另外也可能是交感傳入通路破壞后迷走神經(jīng)中樞功能反射性增強(qiáng)后拮抗所致。 2、交感神經(jīng)調(diào)控不同節(jié)段激活在急性肝損傷早期病程中有促進(jìn)炎癥效應(yīng)。交感神經(jīng)活化可能通過直接作用kupffer細(xì)胞并促進(jìn)炎癥相關(guān)細(xì)胞因子的表達(dá),在一定濃度范圍內(nèi),隨著去甲腎上腺素濃度增加,促炎相關(guān)細(xì)胞因子表達(dá)增加。
[Abstract]:First, the background
In the clinic, due to severe liver trauma, surgery, drug poisoning, bacteria, virus infection induced acute liver injury and other reasons can lead to acute liver failure. The liver function of acute hepatic injury induced by incomplete or acute liver failure, clinical treatment is very difficult, it is difficult to get ideal medicine hepatoprotective effect. This pathology in the process, due to trauma, bacteria, viruses and other direct cause of liver damage is limited, and the body of some minor damage or pathogen inappropriate inflammatory or immune response may cause serious consequences. The inflammatory reaction is too strong so that a large number of inflammatory mediators into the blood circulation can cause systemic inflammatory response syndrome (systemic inflammatory response syndrome, SIRS), caused by shock and multiple system organ failure (multi-system/organ, failure, MSOF), acute liver injury is a systemic inflammatory reaction A viscera manifestation of the syndrome.
The occurrence and development of inflammation is a complex process, influenced by many factors and regulation. Regulatory factors are involved in the inflammatory reaction can be roughly divided into two categories of fluids and nerve, which macrophages play a crucial role in inflammation. The inflammation and liver injury research focus adjustment in the aspect of body fluids, in the study of neural regulation due to the lack of good animal models, fewer studies on display. Hepatic sympathetic regulation system by celiac ganglion, thoracolumbar spinal cord, hypothalamus sympathetic center three different levels of the central composition. Kupffer in liver cells is the main member of monocyte macrophage system, is in residence liver macrophages accounted for more than 80% of the total body macrophages, accounting for 35% of the number of liver nonparenchymal cells, activating.Kupffer cells of the defense function It is closely related to acute liver and chronic inflammation.
Research results at home and abroad in recent years, we conclude that in the occurrence of acute liver injury in the development, along with the change of sympathetic activity, sympathetic nervous system central is entirely possible by adjusting the direct regulation of Kupffer cell expression of inflammatory neurotransmitter release related factors, and thus participate in the start and trigger the excessive inflammatory reaction.
Two, the purpose
This study from different segments of liver sympathetic regulation system to sympathetic treatment, the regulation of the sympathetic nervous system performance of each segment in acute liver injury, and in vitro validation occurs in acute liver injury of sympathetic activation, regulating effect on development. From a new point of view to understand the systemic inflammatory response and the corresponding organ damage regulation mechanism for excessive inflammatory response (SIRS) provides a new way of thinking and the treatment of MODS.
Three, methods and results
1, the influence of different segments of sympathetic denervation on acute liver injury induced by CCL4 in rats: from the cervical sympathetic trunk, splanchnic nerve and nerve endings in the liver of different control section blocking the sympathetic nerve, making the acute liver injury model on the basis of the application of CCL4. The distribution frequency and amplitude changes of electrode determination. Sympathetic with the record of liver function, serum TNF-a level and liver histopathology of liver tissue were measured NE the indexes such as high performance liquid chromatography. The normal rat cervical sympathetic trunk on the wave amplitude of low frequency, uniform voltage stabilized, after CCL4 intraperitoneal injection for liver injury stimulation, sympathetic nerve discharge increased immediately, wave V increases, was pulse enhancement, continuous recording after about 40 seconds, sympathetic nerve activity is back to normal. The waveform of the sympathetic and sympathetic group were compared with shame group in the liver: Albumin and prealbumin increased, AST, ALT, liver function indexes of total bilirubin decreased significantly, the difference was significant (P0.05, P0.01). The greater splanchnic nerve transection and shame group of liver function indexes had no significant difference (P0.05). The TCST group and hepatic sympathetic respectively. Compared with shame group, liver tissue norepinephrine concentrations decreased significantly, very significant difference (P0.01). The greater splanchnic nerve transection and shame were not significantly changed, the statistical difference (P0.05). The transection of cervical sympathetic trunk, to the level of serum TNF-a in liver sympathetic group was significantly lower than that in shame (P0.05), splanchnic nerve transection group was higher than that in shame group.
2, the sympathetic neurotransmitter NE on endotoxin induced by in situ perfusion on expression of Kupffer cell TNF-a/ IL-1 beta rats, type IV collagenase digestion, Percoll density gradient centrifugation and selective adherence method of purified Kupffer cells were divided into three groups (blank control group.A group); B group (LPS); group C (LPS+NE) Real time and ELISA PCR were used to detect the expression of KC TNF- alpha, IL-1 beta and mRNA protein level. KC cells were normally almost no expression of TNF-a and IL-1 beta by exogenous endotoxin LPS (final concentration 10 g/ml) after stimulation of TNF-a increased significantly in 12 hours, the expression of IL-1 beta mRNA; while adding norepinephrine concentration were 1 mol/L and 10 mol/L culture liquid in the treatment group, TNF-a mRNA levels compared with LPS group were increased by 50.9% (P0.05) and 59.1% (P0.05), IL-1 beta mRNA levels increased compared with group LPS 53.7% (P0.05) and 57.8% (P0.05) the expression. The amount and concentration of noradrenaline was positively correlated; the TNF-a IL-1 beta on mRNA and protein level were consistent. Under normal conditions, almost no expression or low expression, LPS (10 g/ml) was increased significantly after stimulation. (LPS+NE) Co stimulation, TNF-a was higher than LPS group IL-1 beta concentration to noradrenaline concentration was 1 mol/L and 10 mol/L (P0.05), and in the low concentration (0.1 mol/L) cases showed no significant difference.
Conclusion:
1, different segments of the sympathetic nervous system to regulate sympathetic nerve, can significantly reduce the damage of liver function in acute liver injury induced by CCL4, liver tissue norepinephrine levels decreased. The sympathetic nervous system of each segment is relatively independent of the control function to control the machine can maintain body stability, also may be the sympathetic afferent pathway damage after the central vagal reflex reinforcement function after induced by antagonistic.
2, the regulation of different segments of sympathetic nerve activation in acute liver injury in early stage can promote the inflammatory effect. Sympathetic nerve activation may directly through Kupffer cells expression of inflammation related cytokines and promote, in a certain range of concentration, with the concentration of noradrenaline increased proinflammatory cytokine expression.

【學(xué)位授予單位】：第三軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2010
【分類號(hào)】：R363

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