Zhu Yonglin, Zhang Luping, Fu Rongzhan, Gao Limin, Feng Guoying, Du Chao, Wang Zhaojie, Yan Xinfeng
Shandong University 27 Shanda Nanlu, Jinan 250100, Shandong, China.
Department of Bone and Joint, Yantai Affiliated Hospital of Binzhou Medical University Yantai 264001, Shandong, China.
Am J Transl Res. 2019 Apr 15;11(4):1938-1947. eCollection 2019.
To investigate endoplasmic reticulum (ER) stress reactions in spinal cord injury rats by evaluating the expression of the glucose-regulated protein 78 (GRP78), C/EBP homologous transcription factor protein (CHOP), X-box binding protein 1 (XBP1), Eif-2α and Bad. SCI models were established using adult female mice. After SCI, the expression of endoplasmic reticulum stress-induced apoptosis proteins were examined in the mice at specific time points using immunohistochemistry and western blot. The results of immunohistochemistry showed that in spinal cord gray matter, Chop, Grp78, XBP1, Eif-2α and Bad were specifically detected in the cytoplasm of the cell. Compare with the SCI group, there was little expression in normal group and sham group. The expression of ER stress-induced apoptosis proteins were significantly increased after spinal cord injury, and the absolute expression was higher than normal group (P < 0.05). Western-Blot results showed that compare with the SCI group, there were little expression of ER stress-induced apoptosis proteins in normal group and sham group. The expression of ER stress-induced apoptosis proteins were significantly increased after spinal cord injury, and the absolute expression was higher than normal group (P < 0.05). These results suggest that some ER stress-induced apoptosis proteins, such as Chop, Grp78, XBP1, Eif-2α and Bad, were activated after spinal cord injury, but the precise regulatory mechanisms remain unclear. In the future, understanding of the precise mechanism of ER stress-mediated apoptosis in SCI may lead to the development of novel treatment strategies.
通过评估葡萄糖调节蛋白78(GRP78)、C/EBP同源转录因子蛋白(CHOP)、X盒结合蛋白1(XBP1)、真核翻译起始因子2α(Eif-2α)和凋亡相关蛋白Bad的表达,研究脊髓损伤大鼠的内质网(ER)应激反应。使用成年雌性小鼠建立脊髓损伤(SCI)模型。脊髓损伤后,在特定时间点通过免疫组织化学和蛋白质印迹法检测小鼠内质网应激诱导的凋亡蛋白的表达。免疫组织化学结果显示,在脊髓灰质中,Chop、Grp78、XBP1、Eif-2α和Bad在细胞胞质中被特异性检测到。与脊髓损伤组相比,正常组和假手术组几乎没有表达。脊髓损伤后内质网应激诱导的凋亡蛋白表达显著增加,且绝对表达高于正常组(P<0.05)。蛋白质印迹结果显示,与脊髓损伤组相比,正常组和假手术组内质网应激诱导的凋亡蛋白几乎没有表达。脊髓损伤后内质网应激诱导的凋亡蛋白表达显著增加,且绝对表达高于正常组(P<0.05)。这些结果表明,脊髓损伤后一些内质网应激诱导的凋亡蛋白,如Chop、Grp78、XBP1、Eif-2α和Bad被激活,但确切的调控机制仍不清楚。未来,了解脊髓损伤中内质网应激介导的凋亡的确切机制可能会导致新的治疗策略的发展。