本文選題：腓腸肌 + 鈍挫傷��； 參考：《山東體育學(xué)院》2015年碩士論文

【摘要】：研究目的:創(chuàng)建大鼠腓腸肌鈍挫傷實(shí)驗(yàn)?zāi)Ｐ?觀(guān)測(cè)大鼠鈍挫傷后線(xiàn)粒體融合-分裂基因的表達(dá)情況,探討大鼠腓腸肌鈍挫傷修復(fù)過(guò)程中線(xiàn)粒體分裂與融合基因表達(dá),闡明腓腸肌損傷后自體修復(fù)中線(xiàn)粒體質(zhì)量控制機(jī)制。研究意義:為下一步從能量代謝角度探討腓腸肌損傷修復(fù)限制因素提供理論基礎(chǔ),為之后研究外源性調(diào)控?fù)p傷修復(fù)速度具有重要意義。研究方法:把60只雄性的健康Wistar大鼠隨機(jī)的分為8個(gè)組別,分別是12h組、2d組、5d組、7d組、10d組、15d組、30d組、對(duì)照組,用自制鈍挫傷打擊器對(duì)前七組Wistar大鼠的兩條后腿的腓腸肌進(jìn)行打擊。前七組依次在大鼠經(jīng)過(guò)鈍挫傷打擊后的12小時(shí)、2天、5天、7天、10天、15天、30天時(shí)即刻取材,對(duì)照組與12小時(shí)組同一天取材,取大鼠兩后腿的腓腸肌,提取總RNA。應(yīng)用RT-PCR技術(shù),以總RNA作為模板,先進(jìn)行反轉(zhuǎn)錄通過(guò)使用逆轉(zhuǎn)錄酶把RNA反轉(zhuǎn)錄成為c DNA,再以c DNA作為模板進(jìn)行PCR的擴(kuò)增反應(yīng),從而得到大鼠線(xiàn)粒體融合-分裂基因的表達(dá)情況。研究結(jié)果:1、12h、2d、5d、7d、10d、15d、30d各組的線(xiàn)粒體融合-分裂基因的表達(dá)情況的總體變化趨勢(shì)表現(xiàn)為:各組與正常對(duì)照組相比顯著性呈現(xiàn)出逐漸降低的趨勢(shì),單看各組間的總體表達(dá)量情況則呈現(xiàn)上升的趨勢(shì)。總趨勢(shì)中2d組、10d組兩個(gè)階段各基因的表達(dá)量在總體上升的趨勢(shì)中均出現(xiàn)了突然下降的情況,2d的基因表達(dá)量達(dá)到最低值,15d、30d的基因表達(dá)量處于最高值。2、在30d時(shí),線(xiàn)粒體融合基因的表達(dá)量均低于正常對(duì)照組,線(xiàn)粒體分裂基因DPR1高于正常對(duì)照組,Fist1低于正常對(duì)照組。3、線(xiàn)粒體融合基因在12h、2d、5d、10d與對(duì)照組相比變化都十分顯著,均顯著下降;線(xiàn)粒體分裂基因僅在2d變化十分顯著。研究結(jié)論:1、線(xiàn)粒體融合-分裂基因的表達(dá)量在2d達(dá)到最低值,處于炎癥反應(yīng)階段,線(xiàn)粒體呼吸受抑制,融合-分裂功能下降,融合基因的表達(dá)量減少導(dǎo)致供能不足,恢復(fù)速率緩慢。線(xiàn)粒體融合分裂基因的表達(dá)量均在10d下降的機(jī)制尚不明確。2、線(xiàn)粒體融合分裂基因的表達(dá)情況總體趨勢(shì)上一致,但線(xiàn)粒體分裂基因的表達(dá)量稍高于融合基因的表達(dá)情況,主要由線(xiàn)粒體分裂基因負(fù)責(zé)調(diào)控細(xì)胞凋亡和能量的重新分配。線(xiàn)粒體的形態(tài)趨于分裂可能是線(xiàn)粒體呼吸功能的下降造成的,同時(shí)線(xiàn)粒體融合基因減少,線(xiàn)粒體分裂基因增多有利于提高代謝效率,為新生細(xì)胞提供足夠的能量。3、在30天時(shí)線(xiàn)粒體融合分裂基因的表達(dá)量趨向于正常水平但總體仍低于正常水平,在修復(fù)期損傷部位的纖維組織和生肌組織同一時(shí)間進(jìn)行增生,此時(shí)線(xiàn)粒體融合水平差能量供應(yīng)不足,使得損傷部位沒(méi)辦法恢復(fù)正常水平狀態(tài),線(xiàn)粒體融合與分裂的動(dòng)態(tài)平衡沒(méi)有達(dá)到最佳水平。線(xiàn)粒體融合-分裂的高度動(dòng)態(tài)平衡對(duì)于細(xì)胞積極有效地適應(yīng)和應(yīng)對(duì)新環(huán)境的變化情況具有重要作用,有利于損傷后的恢復(fù)。
[Abstract]:Objective: to establish an experimental model of blunt gastrocnemius contusion in rats, observe the expression of mitochondrial fusion and mitotic gene after blunt injury of rat gastrocnemius, and investigate the expression of mitochondrial division and fusion gene during the repair of blunt injury of gastrocnemius muscle in rats. To elucidate the mechanism of mitochondrial quality control in autorepair of gastrocnemius after injury. Research significance: to provide a theoretical basis for the further study of the limiting factors of gastrocnemius injury repair from the point of view of energy metabolism, it is of great significance to study the exogenous regulation of injury repair speed. Methods: sixty healthy male Wistar rats were randomly divided into 8 groups: 12 h group, 2 d group, 5 d group, 7 d group, 10 d group, 15 d group, 30 d group, control group. The gastrocnemius muscles of the first seven groups of Wistar rats were attacked with a blunt contusion instrument. The first seven groups were collected immediately after blunt contusion for 12 hours, 7 days, 10 days, 15 days and 30 days. The control group and the 12 hour group were taken from gastrocnemius muscle on the same day, and the total RNA was extracted from the gastrocnemius muscle of both hind legs of the rats. Using RT-PCR technique and total RNA as template, reverse transcription of RNA into c DNA was carried out by reverse transcriptase, then PCR amplification reaction was performed with c DNA as template, and the expression of rat mitochondrial fusion and mitotic gene was obtained. The results showed that the overall trend of mitochondrial fusion and mitotic gene expression in each group was as follows: compared with the control group, the expression of mitochondrial fusion and mitotic gene in each group showed a decreasing trend. The total expression of each group showed an upward trend. In the general trend, the expression of genes in the two stages of 2d group / 10d group showed a sudden decrease in the overall upward trend. The gene expression level of 2d group reached the lowest value at 15d / 30d, and the gene expression level was at the highest value 路2d, and at 30d, the gene expression level of 2d group was at the highest value, and at 30d, the gene expression level of 2d group was at the highest level. The expression of mitochondrial fusion gene was lower than that of normal control group, and the DPR1 of mitotic gene was higher than that of normal control group. The expression of mitochondrial fusion gene was significantly lower than that of control group. Mitochondrial mitotic genes changed significantly only at 2 days. Conclusion: the expression of mitochondrial fusion-mitotic gene reached the lowest level in 2 days. In the stage of inflammation, mitochondrial respiration was inhibited, fusion-division function was decreased, and the expression of fusion gene was decreased, which resulted in insufficient energy supply. The recovery rate is slow. The mechanism of the decrease of mitochondrial fission gene expression at 10 days is unclear. The general trend of mitochondrial fusion cleavage gene expression is consistent, but the expression level of mitochondrial fission gene is slightly higher than that of fusion gene expression. Mitochondrial mitotic genes are responsible for regulating apoptosis and energy redistribution. The decline of mitochondrial respiratory function may be the cause of mitochondrial morphology tending to divide, and the decrease of mitochondrial fusion gene and the increase of mitochondrial fission gene are beneficial to the increase of metabolic efficiency. After 30 days, the expression of Mitochondrial fusion mitotic gene tended to be normal but still below normal level, and proliferated at the same time in the fibrous tissue and muscle tissue of the damaged site during the repair period. At this time, the energy supply of mitochondrial fusion level difference is insufficient, which makes the damaged site unable to return to the normal level, and the dynamic balance between mitochondrial fusion and division does not reach the optimal level. The high dynamic balance of mitochondrial fusion and division plays an important role in adapting to and coping with the changes of the new environment actively and effectively, and is beneficial to the recovery after injury.
【學(xué)位授予單位】：山東體育學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2015
【分類(lèi)號(hào)】：G804.7
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本文編號(hào)：1824026