| 王丹,刘晓娟,康天.内质网应激和未折叠蛋白反应相关分子对儿童自身免疫性脑炎T淋巴细胞的影响[J].安徽医药,2020,24(10):2042-2046. |
| 内质网应激和未折叠蛋白反应相关分子对儿童自身免疫性脑炎T淋巴细胞的影响 |
| Effects of endoplasmic reticulum stress and unfolded protein response related molecules on T lymphocytes in children with autoimmune encephalitis |
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| DOI：10.3969/j.issn.1009?6469.2020.10.032 |
| 中文关键词: 脑炎 内质网应激 毒胡萝卜素 自身免疫性脑炎 T淋巴细胞 细胞凋亡 |
| 英文关键词: Encephalitis Endoplasmic reticulum stress Thapsigargin Autoimmune encephalitis T lymphocyte Apoptosis |
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| 中文摘要: |
| 目的观察内质网应激(Endoplasmic ReticulumStress，ERS)对自身免疫性脑炎(Autoimmune Encephalitis，AE)病人 T淋巴细胞存活和凋亡的影响以及未折叠蛋白反应(Unfolded Protein Response，UPR)信号通路在 AE淋巴细胞存活和死亡中的作用。方法本研究在 2017年 2月至 2019年 2月选取石家庄市第一医院儿科 AE病人和健康供者外周血样本进行研究，并用不同浓度的毒胡萝卜素(Thapsigargin，TG)(浓度为 0、0.5、1、5、10 nM)分别处理 AE病人和健康供者的 T淋巴细胞 48 h，然后利用八肽胆囊收缩素(cholecystokinin octapeptide，CCK?8)实验方法检测细胞存活能力；用 TG(浓度为 5 nM)分别处理 AE病人和健康供者的 T淋巴细胞 48 h，流式细胞仪检测 TG未处理以及 TG处理的 T淋巴细胞的细胞凋亡情况； TG(浓度为 5 nM)刺激 AE病人和健康供者的 T淋巴细胞 48 h，蛋白质印迹法(Western blot)检测 UPR标志分子免疫球蛋白结合蛋白(BIP)和同源蛋白(CHOP)的蛋白表达水平以及凋亡相关蛋白 B淋巴细胞瘤 ?2(Bcl?2)、 B淋巴细胞瘤 ?XL(Bcl?XL)和 bcl?2相关 X蛋白(Bax)表达水平。结果 TG以剂量依赖性抑制 AE病人 T淋巴细胞的增殖，促进 AE病人 T淋巴细胞凋亡，并且使 AE病人 T淋巴细胞的 BIP(0.50±0.05)%比(0.23±0.04)%和抗凋亡蛋白 Bcl?2(1.41±0.04)%比(0.73±0.07)%、Bcl?XL(1.23±0.06)%比(0.51±0.05)%表达下调， CHOP(0.53±0.06)%比(0.81±0.07)%和促凋亡蛋白 Bax(0.51±0.01)%比(1.25±0.05)%的表达水平显著增加。结论内质网应激抑制 AE病人 T淋巴细胞的增殖，促进细胞凋亡，可能通过 BIP和 CHOP来影响细胞凋亡。 |
| 英文摘要: |
| Objective To observe the effect of endoplasmic reticulum stress on the survival and apoptosis of T lymphocytes in AEpatients and the role of unfolded protein response(UPR)signaling pathway in the survival and death of AE lymphocytes.Methods Peripheral blood samples of AE patients and healthy donors from the Department of Pediatrics，Shijiazhuang First Hospital fromFebruary 2017 to February 2019 were collected.T lymphocytes of AE patients and healthy donors were treated with TG at differentconcentrations(0，0.5，1，5，10 nM)for 48h，and then cell viability was tested by cck?8 assay；TG(concentration:5 nM)was used to treat T lymphocytes of AE patients and healthy donors for 48 h，and the apoptosis of untreated and TG treated T lymphocytes was detected by flow cytometry；TG(concentration:5 nM)stimulated T lymphocytes of AE patients and healthy donors for 48 h， and the protein expression levels of UPR marker molecules(Binding immunoglobulin protein，BIP)and(Homologous protein， CHOP)as well as apoptotic related proteins(B?cell lymphoma?2，Bcl?2)，(B?cell lymphoma?XL，Bcl?XL)and(Bcl?2 associated X protein，B，ax)were detected by Western blot.Results TG inhibited the proliferation of T lymphocytes in AE patients in a dose?de? pendent manner，promoted the apoptosis of T lymphocytes in AE patients，and down?regulated the expressions of BIP(0.50±0.05)% vs.(0.23±0.04)% and anti?apoptotic proteins Bcl?2(1.41±0.04)% vs.(0.73±0.07)% and Bcl?XL(1.23±0.06)% vs.(0.51±0.05)%，and significantly increased the expressions of CHOP(0.53±0.06)% vs.(0.81±0.07)% and pro?apoptotic protein Bax(0.51±0.01)% vs.(1.25±0.05)%.Conclusion Endoplasmic reticulum stress inhibits the proliferation of T lymphocytes in AE patients and promotes apoptosis，which may be influenced by BIP and CHOP. |
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