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α1-抗胰蛋白酶对他克莫司诱导的肾损伤的肾保护作用。

Renoprotective Effects of Alpha-1 Antitrypsin against Tacrolimus-Induced Renal Injury.

机构信息

Division of Nephrology, Department of Internal Medicine, School of Medicine, Kyungpook National University, Kyungpook National University Hospital, Daegu 41944, Korea.

出版信息

Int J Mol Sci. 2020 Nov 16;21(22):8628. doi: 10.3390/ijms21228628.

DOI:10.3390/ijms21228628
PMID:33207690
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7696546/
Abstract

The protective effects of alpha-1 antitrypsin (AAT) in tacrolimus (TAC)-induced renal injury was evaluated in a rat model. The TAC group rats were subcutaneously injected with 2 mg/kg TAC every day for four weeks. The TAC with AAT group was cotreated with daily subcutaneous injections of TAC and intraperitoneal injections of AAT (80 mg/kg) for four weeks. The effects of AAT on TAC-induced renal injury were evaluated using serum biochemistry, histopathology, and Western blotting. The TAC injection significantly increased renal interstitial fibrosis, inflammation, and apoptosis as compared to the control treatment. The histopathological examination showed that cotreatment of TAC and AAT attenuated interstitial fibrosis (collagen, fibronectin, and α-SMA staining), and α-SMA expression in Western blotting was also decreased. Immunohistochemical staining for inflammation (osteopontin and ED-1 staining) revealed improved interstitial inflammation in the TAC with AAT group compared to that in the TAC group. The TAC treatment increased renal apoptosis compared to the control treatment, based on the results of increased immunohistochemical staining of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), increased caspase-3 activity, and lower Bcl-2 to Bad expression ratio. However, AAT cotreatment significantly changed these markers and consequently showed decreased apoptosis. AAT protects against TAC-induced renal injury via antifibrotic, anti-inflammatory, and antiapoptotic effects.

摘要

α-1 抗胰蛋白酶（AAT）在他克莫司（TAC）诱导的肾损伤中的保护作用在大鼠模型中进行了评估。TAC 组大鼠每天皮下注射 2mg/kg TAC 共四周。TAC+AAT 组则同时每天皮下注射 TAC 和腹腔内注射 AAT（80mg/kg）共四周。采用血清生化、组织病理学和 Western blot 检测 AAT 对 TAC 诱导的肾损伤的影响。与对照组相比，TAC 注射显著增加了肾间质纤维化、炎症和细胞凋亡。组织病理学检查显示，TAC 和 AAT 联合治疗减轻了间质纤维化（胶原、纤维连接蛋白和 α-SMA 染色），Western blot 中 α-SMA 表达也降低。炎症的免疫组化染色（骨桥蛋白和 ED-1 染色）显示，与 TAC 组相比，TAC+AAT 组的间质炎症得到改善。与对照组相比，TAC 处理增加了肾细胞凋亡，这是基于末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记（TUNEL）免疫组化染色增加、caspase-3 活性增加和 Bcl-2 对 Bad 表达比值降低的结果。然而，AAT 联合治疗显著改变了这些标志物，从而显示出凋亡减少。AAT 通过抗纤维化、抗炎和抗凋亡作用来保护 TAC 诱导的肾损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3a1/7696546/e15b23f57208/ijms-21-08628-g008.jpg
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