【摘要】：目的: 建立大鼠宮內(nèi)感染模型,研究外源褪黑素(melatonin,MT)對(duì)LPS致宮內(nèi)感染胎鼠腦組織氧化損傷及TNF-α的表達(dá)變化,并探討MT對(duì)宮內(nèi)感染胎鼠腦組織的保護(hù)作用。 方法: 選用妊娠第19天SD大鼠隨機(jī)分組,對(duì)照組(S組)、宮內(nèi)感染組(LPS組)和MT處理組(MT組)。通過(guò)給孕鼠腹腔注射細(xì)菌脂多糖(1ipopolysaccharide,LPS)造成大鼠宮內(nèi)感染模型。LPS組和S組分別予腹腔注射LPS(500μg/kg)和等容積生理鹽水;MT處理組孕鼠同時(shí)腹腔注射LPS 500μg/kg +MT 10mg/kg。根據(jù)注藥后觀察時(shí)間不同,將各組孕鼠分為注藥后1h、6h、12h、24h、48h、72h共6個(gè)時(shí)間點(diǎn),每個(gè)時(shí)間點(diǎn)4只孕鼠,于相應(yīng)的時(shí)間點(diǎn)迅速處死孕鼠,冰盒上剖腹取胎并隨機(jī)取出8只胎鼠腦組織,分別測(cè)定腦組織勻漿的MDA活力和GSH-Px含量,采用RT-PCR技術(shù)檢測(cè)胎鼠腦組織中TNF-αmRNA的水平表達(dá)情況,并比較各組之間的差異。 結(jié)果: 1、成功構(gòu)建了宮內(nèi)感染胎鼠腦損傷模型。 2、隨感染時(shí)間延長(zhǎng),宮內(nèi)感染組較對(duì)照組胎鼠腦組織中MDA活力上升,GSH-Px含量下降,TNF-αmRNA含量則是先升后降;同時(shí)隨著感染時(shí)間的延長(zhǎng),上述改變趨于明顯(P0.05)。 3、外源MT能使宮內(nèi)感染胎鼠腦組織中MDA活力顯著降低,明顯升高GSH-Px含量,TNF-αmRNA水平顯著下降,且均有統(tǒng)計(jì)學(xué)意義(P 0.05)。 結(jié)論: 1、通過(guò)給孕鼠腹腔注射脂多糖成功建立了宮內(nèi)感染模型并可致胎鼠腦損傷,表明宮內(nèi)感染是導(dǎo)致胎鼠腦損傷的重要因素之一。 2、宮內(nèi)感染致胎鼠腦組織存在氧化損傷、腦神經(jīng)損傷增多,同時(shí)一定時(shí)間內(nèi),隨著感染時(shí)間的延長(zhǎng)而逐漸加重。 3、褪黑素對(duì)宮內(nèi)感染胎鼠腦組織有抗氧化、抗損傷的作用,并能抑制和降低宮內(nèi)感染誘導(dǎo)的炎癥因子的增加,表明褪黑素對(duì)宮內(nèi)感染胎鼠腦組織有保護(hù)作用。
[Abstract]:Aim: to establish a rat model of intrauterine infection and to study the effects of exogenous melatonin (MT) on oxidative damage and expression of TNF- 偽 in fetal brain tissue induced by lipopolysaccharide (LPS), and to explore the protective effect of MT on fetal brain tissue infected with intrauterine infection. Methods: SD rats on the 19th day of pregnancy were randomly divided into control group (S group), intrauterine infection group (LPS group) and MT treatment group (MT group). Intraperitoneal injection of lipopolysaccharide (LPS) by intraperitoneal injection of lipopolysaccharide (LPS) in pregnant rats. The intrauterine infection model of rats was induced by intraperitoneal injection of lipopolysaccharide (LPS). Group S and group S were treated by intraperitoneal injection of LPS (500 渭 g/kg) and intraperitoneal injection of LPS 500 渭 g/kg MT (10 mg / kg) at the same time. According to the different observation time, the pregnant rats in each group were divided into 6 time points at 1h, 6h, 12h, 24h, 48h and 72h. At each time point, 4 pregnant rats were killed quickly at the corresponding time points. The fetal tissues were taken out by caesarean section on the ice box and 8 fetal brain tissues were taken out at random. The activity of MDA and the content of GSH-Px in brain homogenate were measured, and the expression of TNF- 偽 mRNA in fetal brain tissue was detected by RT-PCR. Results: 1. The rat model of fetal brain injury caused by intrauterine infection was successfully constructed. (2) with the prolongation of the time of infection, the content of GSH-Px in the intrauterine infection group was lower than that in the control group, and the content of TNF- 偽 mRNA increased first and then decreased; At the same time, with the extension of infection time, the above changes tended to be obvious (P0.05). Exogenous MT could significantly decrease the activity of MDA and increase the content of GSH-Px and decrease the level of TNF- 偽 mRNA significantly (P 0.05). Conclusion: 1. Intrauterine infection model was successfully established by intraperitoneal injection of lipopolysaccharide into pregnant rats, and fetal brain injury was induced. The results indicate that intrauterine infection is one of the important factors leading to fetal brain injury. With the prolongation of infection time, melatonin can inhibit and decrease the increase of inflammatory factors induced by intrauterine infection. These results suggest that melatonin has protective effect on fetal brain tissue infected by intrauterine infection.
【學(xué)位授予單位】：蘇州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2011
【分類號(hào)】：R363

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