【摘要】： 目的：研究?jī)煞N不同劑量的鏈霉素?fù)p傷后,小鼠前庭感覺(jué)上皮中毛細(xì)胞再生情況。 方法：通過(guò)左耳后半規(guī)管將兩種不同劑量的鏈霉素注入小鼠前庭,分別建立小鼠前庭感覺(jué)上皮中度和重度損傷模型。術(shù)后不同時(shí)間點(diǎn)行橢圓囊免疫熒光染色、掃描電鏡和樹(shù)脂切片,觀察不同程度損傷后橢圓囊感覺(jué)上皮的形態(tài)特征及毛細(xì)胞再生情況。 結(jié)果：橢圓囊前庭感覺(jué)上皮中度損傷后,毛細(xì)胞嚴(yán)重缺失,支持細(xì)胞保存良好；損傷后2周內(nèi)出現(xiàn)以幼小纖毛為特征的新生毛細(xì)胞,并隨著時(shí)間延長(zhǎng)而增多；但是新生毛細(xì)胞的形態(tài)有別于正常毛細(xì)胞,而且再生的毛細(xì)胞數(shù)目有限。重度損傷后,毛細(xì)胞和支持細(xì)胞均受到嚴(yán)重?fù)p害,前庭感覺(jué)上皮被一極薄的單層扁平上皮取代；毛細(xì)胞的自我再生能力較中度損傷時(shí)極度減弱；部分細(xì)胞無(wú)毛細(xì)胞或支持細(xì)胞的特征。 結(jié)論：鏈霉素?fù)p傷后,小鼠前庭感覺(jué)上皮具有有限的自我再生能力。重度損傷極度降低了這種再生能力,前庭感覺(jué)上皮被一極薄的單層扁平上皮取代。 目的：探討小鼠前庭毛細(xì)胞再生過(guò)程中Notch信號(hào)途徑因子和Atoh1的作用。 方法：通過(guò)后半規(guī)管途徑將鏈霉素注入小鼠前庭,建立小鼠前庭感覺(jué)上皮中度損傷模型。然后我們分別用免疫熒光染色和實(shí)時(shí)定量PCR的方法檢測(cè)橢圓囊前庭感覺(jué)上皮中Notch信號(hào)途徑因子(Notch1, Jagged1, Hes1, Hes5)及Atoh1的蛋白和mRNA的表達(dá)。 結(jié)果：免疫組化結(jié)果顯示Jagged1表達(dá)于正常和損傷后支持細(xì)胞的細(xì)胞膜；Atoh1在正常小鼠前庭感覺(jué)上皮中無(wú)表達(dá),但是毛細(xì)胞損傷后Atoh1表達(dá)增高,并可伴有myosinⅦa的共表達(dá)。實(shí)時(shí)定量PCR結(jié)果顯示小鼠前庭毛細(xì)胞再生過(guò)程中Hes5下降,Atohl上升,Notch1, Jagged1和Hes1無(wú)變化。 結(jié)論：Notch信號(hào)通路和Atoh1參與了小鼠前庭毛細(xì)胞損傷后的自我再生過(guò)程。再生的啟動(dòng)時(shí)間可能早于過(guò)去的觀點(diǎn),Atoh1的升高可能是多條信號(hào)通路共同作用的結(jié)果。 目的：研究?jī)煞N不同劑量的鏈霉素?fù)p傷后,小鼠前庭感覺(jué)上皮中神經(jīng)突觸、神經(jīng)纖維和前庭神經(jīng)節(jié)神經(jīng)元的變化。 方法：通過(guò)后半規(guī)管將兩種不同劑量的鏈霉素注入小鼠前庭,分別建立小鼠前庭感覺(jué)上皮中度和重度損傷模型。神經(jīng)絲蛋白200抗體免疫熒光染色觀察損傷后不同時(shí)間點(diǎn)橢圓囊前庭感覺(jué)上皮中神經(jīng)突觸和神經(jīng)纖維的變化；上前庭神經(jīng)節(jié)神經(jīng)元樹(shù)脂切片及定量分析,評(píng)價(jià)神經(jīng)元的存活情況。 結(jié)果：中度損傷和重度損傷后1月,神經(jīng)盞損傷嚴(yán)重,但是神經(jīng)纖維存活,上前庭神經(jīng)節(jié)神經(jīng)元形態(tài)正常,密度無(wú)明顯改變；重度損傷后3月,扁平上皮中無(wú)神經(jīng)盞,上前庭神經(jīng)節(jié)神經(jīng)元的密度明顯下降。 結(jié)論：小鼠前庭感覺(jué)上皮損傷后,神經(jīng)支配退化緩慢。這為干細(xì)胞移植或人工前庭植入研究提供了有利條件。
[Abstract]:Aim: to study the regeneration of hair cells in vestibular sensory epithelium of mice after two different doses of streptomycin. Methods: two different doses of streptomycin were injected into the vestibular of mice through the posterior semicircular canal of the left ear to establish the model of moderate and severe vestibular sensory epithelium injury. Immunofluorescence staining, scanning electron microscopy and resin sections were performed at different time points after operation to observe the morphological characteristics of sensory epithelium and hair cell regeneration after different degrees of injury. Results: after moderate injury of sensory epithelium of ovale vesicles, hair cells were seriously absent and Sertoli cells were well preserved, and new hair cells with the characteristics of young cilia appeared within 2 weeks after injury, and increased with the prolongation of time. However, the morphology of new hair cells is different from that of normal hair cells, and the number of regenerated hair cells is limited. After severe injury, both hair cells and Sertoli cells were seriously damaged, the vestibular sensory epithelium was replaced by a very thin monolayer flat epithelium, and the ability of self-regeneration of hair cells was extremely weakened when the injury was moderate. Characteristics of hairless cells or Sertoli cells in some cells. Conclusion: the vestibular sensory epithelium of mice has limited ability of self-regeneration after streptomycin injury. Severe injury greatly reduces this ability to regenerate and the vestibular sensory epithelium is replaced by a very thin monolayer flattened epithelium. Aim: to investigate the role of Notch signal pathway factor and Atoh1 in the regeneration of mouse vestibular hair cells. Methods: streptomycin was injected into the vestibule of mice through the posterior semicircular canal pathway to establish the model of moderate vestibular sensory epithelial injury in mice. Then immunofluorescence staining and real-time quantitative PCR were used to detect the expression of Notch signal pathway factor (Notch1, Jagged1, Hes1, Hes5), Atoh1 protein and mRNA in the vestibular sensory epithelium of elliptic sac. Results: the results of immunohistochemistry showed that Jagged1 was expressed in the membrane of Sertoli cells after injury and normal mice, but there was no expression of Atoh1 in vestibular sensory epithelium of normal mice, but the expression of Atoh1 was increased after hair cell injury with co-expression of myosin 鈪，

本文編號(hào)：2467656