本文選題：促甲狀腺激素釋放激素 + 促甲狀腺激素釋放激素受體��； 參考：《第四軍醫(yī)大學(xué)》2008年博士論文

【摘要】： 背景與目的 促甲狀腺激素釋放激素(thyrotrophin-releasing hormone, TRH)最初是從羊和豬的下丘腦中提取并純化的3肽,它與垂體前葉促甲狀腺激素細(xì)胞表面特異性受體(thyrotrophin-releasing hormone receptors, TRHRs)結(jié)合,刺激促甲狀腺激素(TSH)的合成和分泌。在哺乳動(dòng)物體內(nèi)先后克隆出了針對(duì)TRH的兩個(gè)受體,TRH-R1和TRH-R2,兩者同屬G蛋白耦聯(lián)受體家族成員,在同種動(dòng)物中其氨基酸序列具有50%的一致性。具有免疫活性的TRH及TRH受體不僅分布于下丘腦及其以外的中樞神經(jīng)系統(tǒng)內(nèi),還廣泛存在于外周組織中。睪丸是外周組織中為數(shù)不多的可同時(shí)表達(dá)TRH及其兩個(gè)受體的器官,但TRH及其受體在睪丸內(nèi)的功能尚不清楚,因而本實(shí)驗(yàn)的目的在于探討TRHRs在大鼠睪丸內(nèi)表達(dá)的意義。 研究方法和內(nèi)容 1.利用蛋白質(zhì)免疫印跡雜交及免疫組織化學(xué)方法對(duì)比研究出生后大鼠發(fā)育不同階段(8,14,21,35,60和90天)睪丸中TRH-R2和TRH-R1的表達(dá)和定位,并結(jié)合圖像分析技術(shù)對(duì)其表達(dá)進(jìn)行半定量分析。 2.采用Percoll連續(xù)密度梯度法離心法提取、純化并原代培養(yǎng)成年大鼠(90天)睪丸Leydig細(xì)胞,探討不同劑量TRH對(duì)Leydig細(xì)胞睪酮合成的影響。 3.合成EDS,構(gòu)建并驗(yàn)證EDS誘導(dǎo)的Leydig細(xì)胞凋亡模型;采用Western blotting、免疫組織化學(xué)以及免疫熒光雙標(biāo)的方法,觀察在EDS處理后成年型Leydig細(xì)胞再生過(guò)程中TRH-R1和TRH-R2的表達(dá)情況。 4.從出生后21d大鼠睪丸內(nèi)分離、純化Leydig祖細(xì)胞,采用BrdU摻入實(shí)驗(yàn),觀察不同劑量的TRH對(duì)Leydig祖細(xì)胞DNA合成的影響。 結(jié)果 1.Western blotting和免疫組織化學(xué)均檢測(cè)到了TRH-R1和TRH-R2在大鼠睪丸出生后不同階段的表達(dá),定位在Leydig細(xì)胞,陽(yáng)性物質(zhì)位于胞漿和胞膜,同一個(gè)Leydig細(xì)胞可同時(shí)表達(dá)TRH-R1和TRH-R2。圖像分析顯示兩者在不同階段Leydig細(xì)胞內(nèi)的表達(dá)強(qiáng)度有所不同,TRH-R2最大表達(dá)量為出生后35d睪丸,主要為新形成及未成熟的Leydig細(xì)胞,而TRH-R1則在成年大鼠睪丸內(nèi)表達(dá)較高,主要為成熟的Leydig細(xì)胞。 2.Percoll連續(xù)密度梯度離心法提取成年大鼠睪丸Leydig細(xì)胞,經(jīng)3β-HSD酶細(xì)胞化學(xué)染色,純度符合細(xì)胞學(xué)實(shí)驗(yàn)要求。在給予不同劑量TRH處理后,原代培養(yǎng)的Leydig細(xì)胞睪酮分泌受到影響,并呈劑量依賴性。相對(duì)低劑量的TRH(0.01和0.1 ng/ml)可顯著抑制ALCs基礎(chǔ)睪酮和hCG刺激下的睪酮分泌,P值小于0.01;而相對(duì)高劑量的TRH(1和10 ng/ml)卻促進(jìn)了hCG刺激下的睪酮分泌(P0.05)。雖然1 ng/ml TRH組與0.1 ng/ml TRH在基礎(chǔ)睪酮分泌上沒(méi)有統(tǒng)計(jì)學(xué)差異,1 ng/ml TRH刺激下,ALCs睪酮水平亦有所升高。 3.按照75mg/kg的劑量一次性給予大鼠腹腔注射EDS后,睪丸Leydig細(xì)胞在2 d后可全部凋亡消失,經(jīng)血清睪酮測(cè)量、睪丸恒冷箱切片3β-HSD酶細(xì)胞化學(xué)染色、石蠟切片HE染色以及3β-HSD的免疫組織化學(xué)染色等證實(shí),動(dòng)物模型復(fù)制成功。一次性腹腔注射EDS后,Leydig細(xì)胞在24hr內(nèi)即發(fā)生退化,2-3天后,Leydig細(xì)胞全部消失。EDS處理后14d,在間質(zhì)管周區(qū)出現(xiàn)長(zhǎng)梭形Leydig細(xì)胞的再生,至處理后28d新生的Leydig細(xì)胞數(shù)量增加并由管周向間質(zhì)中央遷移,變?yōu)槎嘟切巍?在EDS處理后的14d,Western blotting和免疫組織化學(xué)染色檢測(cè)到了TRH-R1和TRH-R2在睪丸內(nèi)的表達(dá),此時(shí)對(duì)應(yīng)著大鼠睪丸Leydig祖細(xì)胞的再生,經(jīng)利用熒光雙標(biāo)進(jìn)一步證實(shí),TRH-R1和TRH-R2陽(yáng)性細(xì)胞即為再生的Leydig細(xì)胞。 4.采用Percoll連續(xù)密度梯度離心法從出生后14d大鼠中成功分離、純化了Leydig祖細(xì)胞。在給予不同劑量的TRH(0.001-10 ng/ml)并向培養(yǎng)液中添加10μM BrdU后,PLCs的DNA合成可受到TRH的影響。在孵育12小時(shí)后,相對(duì)低劑量的TRH(0.001-0.1 ng/ml)可增加BrdU陽(yáng)性標(biāo)記細(xì)胞的數(shù)量和比例(從8.2%升高至11%以上),即PLCs的DNA合成增加,細(xì)胞的增殖或分化可能增多。但是相對(duì)高劑量的TRH(1 ng/ml)卻不能促進(jìn)PLCs的DNA合成,甚至BrdU摻入比例在10ng/ml TRH組略有下降(P=0.094)。將BrdU摻入時(shí)間延長(zhǎng)至18和36hr,對(duì)照組和TRH處理組BrdU陽(yáng)性細(xì)胞的數(shù)量和比例均增加(P0.01),即0.1ng/ml TRH可顯著促進(jìn)PLCs的DNA合成。 結(jié)論 1.成功分離、純化了大鼠睪丸PLCs和ALCs,可用于原代培養(yǎng)下細(xì)胞學(xué)實(shí)驗(yàn)。 2.成功合成EDS,并構(gòu)建EDS誘導(dǎo)的成年大鼠Leydig細(xì)胞凋亡-再生模型。 3.TRH-R1和TRH-R2在大鼠睪丸出生后發(fā)育不同階段以及EDS誘導(dǎo)的Leydig細(xì)胞凋亡模型中僅表達(dá)于Leydig細(xì)胞,即處于成年型Leydig細(xì)胞譜系不同階段的Leydig細(xì)胞均表達(dá)TRH-R1和TRH-R2。另外,細(xì)胞培養(yǎng)顯示,TRH能夠影響成熟的ALCs睪酮合成分泌能力,以及Leydig祖細(xì)胞的DNA合成(增殖或分化)。故TRH及其受體參與了Leydig細(xì)胞譜系的發(fā)育和功能的調(diào)節(jié)。
[Abstract]:Background and purpose
Thyrotrophin-releasing hormone (TRH) is originally a 3 peptide extracted and purified from the hypothalamus of sheep and pigs. It combines with the thyrotrophin-releasing hormone receptors (TRHRs) receptor (thyrotrophin-releasing hormone receptors, TRHRs) in the anterior pituitary and stimulates the synthesis and secretion of thyroid stimulating hormone (TSH). Two receptors for TRH, TRH-R1 and TRH-R2, are cloned in the milk moving object, and both belong to the family members of the G protein coupling receptor family. The amino acid sequences of the same animals are consistent in the same animals. The immune active TRH and TRH receptors are distributed not only in the central nervous system of the hypothalamus and outside the hypothalamus, but also in the peripheral area. In the tissue, the testicles are the few organs in the peripheral tissue that can simultaneously express TRH and its two receptors, but the function of TRH and its receptors in the testis is not clear. The purpose of this experiment is to explore the significance of TRHRs expression in the testis of rats.
Research methods and contents
1. the expression and localization of TRH-R2 and TRH-R1 in the testis of the postnatal rats (8,14,21,35,60 and 90 days) were compared by the method of protein immunoblot hybridization and immunohistochemistry, and the expression was semi quantified by image analysis.
2. the Percoll continuous density gradient centrifugation was used to extract and purify the adult rat (90 days) rat testicular Leydig cells, and to explore the effect of different doses of TRH on the testosterone synthesis of Leydig cells.
3. EDS was synthesized and the EDS induced Leydig cell apoptosis model was constructed and verified. The expression of TRH-R1 and TRH-R2 during the regeneration of adult Leydig cells after EDS treatment was observed by Western blotting, immunohistochemistry and double immunofluorescence.
4. the Leydig progenitor cells were purified from the testis of 21d rats after birth, and the effects of different doses of TRH on the DNA synthesis of Leydig progenitor cells were observed by BrdU incorporation.
Result
1.Western blotting and immunohistochemistry detected the expression of TRH-R1 and TRH-R2 at different stages after the birth of the rat testis, located in the Leydig cells, the positive substance was located in the cytoplasm and the cytoplasm, and the same Leydig cell could simultaneously express the TRH-R1 and TRH-R2. image analysis to show that the expression intensity of the two in the different stages of Leydig cells in different stages. The largest expression of TRH-R2 is the postnatal 35d testis, mainly new and immature Leydig cells, while TRH-R1 is highly expressed in the testis of adult rats, mainly the mature Leydig cells.
2.Percoll continuous density gradient centrifugation was used to extract Leydig cells from adult rat testicles. After 3 beta -HSD enzyme cytochemical staining, the purity accords with the requirement of cytological experiment. After the treatment of different doses of TRH, the secretion of testosterone in the primary cultured Leydig cells is affected and is dose-dependent. The relative low dose of TRH (0.01 and 0.1 ng/ml) can be significantly inhibited. The testosterone secretion of ALCs based testosterone and hCG was less than 0.01, while the relative high dose of TRH (1 and 10 ng/ml) promoted the testosterone secretion under hCG stimulation (P0.05). Although the 1 ng/ml TRH group and 0.1 ng/ml TRH were not statistically different from the basal testosterone secretion, the level of testosterone was also elevated under 1 ng/ml.
3. after an intraperitoneal injection of EDS in rats at a dose of 75mg/kg, the apoptosis of Leydig cells in the testis disappeared after 2 D. By serum testosterone, 3 beta -HSD enzyme cytochemical staining, HE staining in paraffin section and immunohistochemical staining of 3 beta -HSD were confirmed by serum testosterone, and the animal model was replicated successfully. After EDS, Leydig cells degenerated within 24hr. After 2-3 days, all Leydig cells disappeared after.EDS treatment and 14d. The regeneration of long shuttle shaped Leydig cells appeared in the periinterstitial region. The number of Leydig cells in the newborn 28d increased and migrated from the peritubule to the mesenchyme, and turned into polygons.
The expression of TRH-R1 and TRH-R2 in the testis was detected by 14d, Western blotting and immunohistochemical staining after EDS treatment. At this time, the regeneration of Leydig progenitor cells in the rat testis was regenerated. It was further confirmed by double labeling fluorescence, that TRH-R1 and TRH-R2 positive cells were regenerated Leydig cells.
4. the Percoll continuous density gradient centrifugation was used to separate the Leydig progenitor cells from the postnatal 14d rats. After giving different doses of TRH (0.001-10 ng/ml) and adding 10 mu M BrdU to the culture medium, the PLCs DNA synthesis could be influenced by TRH. After 12 hours of incubation, the relatively low dose TRH could increase the positive rate. The number and proportion of the sex labeled cells (from 8.2% to more than 11%), that is, the DNA synthesis of PLCs increases, cell proliferation or differentiation may increase. But the relative high dose of TRH (1 ng/ml) does not promote DNA synthesis of PLCs, even the proportion of BrdU admixture decreases slightly in the 10ng/ml TRH group (P=0.094). The BrdU incorporation time is extended to 18 and 36hr, control, and 36hr, control The number and proportion of BrdU positive cells in both group and TRH treated group increased (P0.01), that is, 0.1ng/ml TRH significantly promoted DNA synthesis of PLCs.
conclusion
1. successfully isolated and purified PLCs and ALCs from rat testis, which can be used in primary culture cytology experiments.
2. EDS was successfully synthesized, and EDS induced apoptosis and regeneration model of adult rat Leydig cells was constructed.
3.TRH-R1 and TRH-R2 were expressed only in Leydig cells in the different stages of the development of rat testis and in the Leydig cell apoptosis induced by EDS, that is, the Leydig cells in the different stages of the adult Leydig cell lineage all express TRH-R1 and TRH-R2., and the cell culture shows that TRH can affect the capacity of the mature ALCs testosterone synthesis and secretion. And DNA synthesis (proliferation or differentiation) of Leydig progenitor cells. Therefore, TRH and its receptors are involved in the regulation of Leydig cell lineage development and function.
【學(xué)位授予單位】：第四軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2008
【分類號(hào)】：R329

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