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田 勇,董其娟,于江红,韩 超.胰激肽原酶对糖尿病大鼠视网膜病变的保护作用及对 Notch1 / Hes-1 信号通路的影响[J].中国比较医学杂志,2021,31(5):102~107,127.
胰激肽原酶对糖尿病大鼠视网膜病变的保护作用及对 Notch1 / Hes-1 信号通路的影响
The protective effect of pancreatic kininogenase on the retinopathy of diabetic rats and its influence on the Notch1 / Hes-1 signaling pathway
投稿时间:2020-08-08  
DOI:10. 3969 / j.issn.1671-7856. 2021. 05. 017
中文关键词:  糖尿病  视网膜神经节细胞  胰激肽原酶  Notch1 / Hes-1 信号通路  大鼠
英文关键词:diabetes  retinal ganglion cells  pancreatic kininogenase  Notch1 / Hes-1 signaling pathway  rats
基金项目:
作者单位E-mail
田 勇 河南中医药大学人民医院(郑州人民医院)内分泌代谢科,郑州 450003 xin5482g@ 163.com 
董其娟 河南中医药大学人民医院(郑州人民医院)内分泌代谢科,郑州 450003  
于江红 河南中医药大学人民医院(郑州人民医院)内分泌代谢科,郑州 450003  
韩 超 郑州大学第一附属医院临床药学科,郑州 450052  
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中文摘要:
       目的 观察胰激肽原酶对糖尿病(diabetes mellitus,DM)大鼠视网膜病变的保护作用,并探究其作用机制。 方法 将 60 只 SPF 级大鼠随机分为空白组、模型组和治疗组,每组 20 只。模型组和治疗组通过单次腹腔注射 60 mg / kg 链脲佐菌素(streptozocin,STZ)建立 DM 模型,空白组腹腔注射等量 0. 1 moL/ L 枸橼酸钠。治疗组腹腔注射胰激肽原酶 0. 8 U 治疗,空白组和模型组腹腔注射 0. 2 mL 生理盐水,每天 1 次,连续 2 周。 HE 染色观察大鼠视网膜神经节细胞( retinal ganglion cells,RGCs)病理学变化并计数;TUNEL 法检测 RGCs 凋亡情况;ELISA 试剂盒检测视网膜组织 SOD 活力和 MDA 含量;qRT-PCR 法和 Western blot 法检测视网膜组织 Notch-1、Hes-1 mRNA 和蛋白表达。 结果 空白组大鼠视网膜组织各层结构清晰,RGCs 细胞核清晰有序,偶见凋亡细胞;与空白组比较,模型组 RGCs 排列紊乱,细胞核稀疏,RGCs 数量显著减少,凋亡率升高,视网膜组织 SOD 水平降低,MDA 含量升高(P<0. 05);与模型组比较,治疗组视网膜组织各层结构清晰,RGCs 细胞核清晰规整,RGCs 层细胞数量增加,凋亡率降低,视网膜组织 SOD 活力提高,MDA 含量降低(P<0. 05)。 qRT-PCR 和 Western blot 检测结果显示,与空白组比较, 模型组视网膜组织 Notch1、Hes1 mRNA 和蛋白表达水平降低(P<0. 05);与模型组比较,治疗组视网膜组织 Notch1、 Hes1 mRNA 和蛋白表达水平升高(P<0. 05)。 结论 胰激肽原酶对 DM 大鼠视网膜病变具有保护和改善作用,其作用机制可能与激活 Notch1 / Hes-1 信号通路的表达有关。
英文摘要:
       Objective To examine the protective effect of pancreatic kininogenase on retinopathy in diabetes mellitus rats, and explore its mechanism of action. Methods Sixty specific-pathogen-free rats were randomly divided into a blank group, model group, and treatment group, with 20 rats in each group. The model group and treatment group were given a single intraperitoneal injection of 60 mg / kg streptozotocin to establish a rat diabetes model. Rats in the blank group were intraperitoneally injected with an equivalent amount of 0. 1 moL/ L sodium citrate. Rats in the treatment group were treated by intraperitoneal injection of 0. 8 U of pancreatic kininogenase, while the blank group and model group were intraperitoneally injected with 0. 2 mL of normal saline once a day for 2 weeks. Hematoxylin and eosin staining was used to observe pathological changes of retinal ganglion cells ( RGCs). Apoptosis of RGCs was detected by TUNEL staining. Activity of superoxide dismutase ( SOD) and malondialdehyde ( MDA) content in the retina were detected by enzyme- linked immunosorbent assay. mRNA and protein expression of Notch1 and HES-1 were detected by quantitative RT-PCR and western blotting. Results In the blank group, the structure of each layer of retinal tissue was clear, RGC nuclei were clear and orderly, and apoptotic cells were only occasionally seen. Compared with the blank group, RGCs in the model group were arranged disorderly, the nuclei were sparse, the number of RGCs was significantly reduced, apoptosis rate was increased, SOD activity of retinal tissue was decreased, and MDA content was increased (P< 0. 05). Compared with the model group, the structure of each layer of retinal tissue in the treatment group was clear, the nuclei of RGCs were clear and regular, the number of RGC layer cells was increased, apoptosis rate was decreased, SOD activity of retinal tissue was increased, and content of MDA was decreased (P< 0. 05). The quantitative RT-PCR and western blotting result showed that mRNA and protein expression levels of Notch1 and Hes1 were decreased in the model group compared with the blank group (P< 0. 05). Compared with the model group, mRNA and protein expression levels of Notch1 and Hes1 in the treatment group were increased ( P< 0. 05). Conclusions Pancreatic kininogenase can protect and improve diabetic retinopathy. The mechanism may be related to the activation of the Notch1 / HES-1 signaling pathway.
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