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實(shí)驗(yàn)性自身免疫性重癥肌無(wú)力模型大鼠腓腸肌低密度脂蛋白受體相關(guān)蛋白4表達(dá)的特點(diǎn)

發(fā)布時(shí)間:2018-04-19 11:07

  本文選題:低密度脂蛋白受體相關(guān)蛋白 + 重癥肌無(wú)力 ; 參考:《臨床神經(jīng)病學(xué)雜志》2017年02期


【摘要】:目的探討實(shí)驗(yàn)性自身免疫性重癥肌無(wú)力(EAMG)模型大鼠腓腸肌低密度脂蛋白受體相關(guān)蛋白4(LRP4)表達(dá)的特點(diǎn)。方法將30只大鼠隨機(jī)分為EAMG組、對(duì)照組和空白組。以小鼠乙酰膽堿受體(AChR)基因?yàn)槟0搴铣葾ChR抗原,以L(fǎng)ewis大鼠為免疫動(dòng)物。EAMG組采取主動(dòng)免疫法將AChR抗原與弗氏佐劑混合制成乳劑,注射入大鼠背部皮下。對(duì)照組在相同部位注射等量的弗氏佐劑?瞻捉M在相同部位注射等量的生理鹽水。8周后使用低頻重復(fù)電刺激(RNS)檢測(cè)肌電RNS衰減率。采用蛋白免疫印跡法檢測(cè)腓腸肌LRP4含量。結(jié)果 EAMG組所有大鼠在8周后出現(xiàn)肌無(wú)力癥狀,對(duì)照組、空白組大鼠無(wú)肌無(wú)力癥狀。EAMG組大鼠RNS衰減率明顯高于對(duì)照組和空白組(均P0.05)。EAMG組大鼠腓腸肌LRP4蛋白的相對(duì)含量明顯低于對(duì)照組和空白組(均P0.05)。結(jié)論 EAMG大鼠中,當(dāng)AChR被自身抗體破壞時(shí),可能導(dǎo)致包含LRP4在內(nèi)的整條信號(hào)通路受損,進(jìn)而使LRP4含量減少。LRP4是神經(jīng)肌肉接頭信號(hào)通路完整的重要分子。
[Abstract]:Objective to investigate the expression of low density lipoprotein receptor associated protein (LRP4) in gastrocnemius muscle of experimental autoimmune myasthenia gravis rats.Methods 30 rats were randomly divided into EAMG group, control group and blank group.The AChR antigens were synthesized from the acetylcholine receptor (ache) group of mice. The Lewis rats were used as immune animals. The EAMG group prepared the emulsion with the mixture of AChR antigen and Freund's adjuvant by active immune method, and injected into the back of the rats subcutaneously.The control group received the same dose of Freund's adjuvant at the same site.Low frequency repetitive electrical stimulation (RNS) was used to detect the RNS attenuation rate in the blank group after injection of the same amount of normal saline at the same site for 8 weeks.The content of LRP4 in gastrocnemius muscle was detected by Western blot.Results all the rats in EAMG group developed myasthenia after 8 weeks.The attenuation rate of RNS in control group and blank group was significantly higher than that in control group and blank group. The relative content of LRP4 protein in gastrocnemius muscle in P0.05).EAMG group was significantly lower than that in control group and blank group (all P 0.05).Conclusion in EAMG rats, when AChR is destroyed by autoantibodies, the whole signal pathway including LRP4 may be damaged, and the decrease of LRP4 content. LRP4 is an important molecule in the complete signal pathway of neuromuscular junction.
【作者單位】: 河南省濮陽(yáng)市人民醫(yī)院神經(jīng)內(nèi)科;河北醫(yī)科大學(xué)第二附屬醫(yī)院神經(jīng)內(nèi)科;
【分類(lèi)號(hào)】:R746.1;R-332

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