Antithrombin III prevents progression of chronic kidney disease following experimental ischaemic‐reperfusion injury
Autor: | Jianyong Yin, Yiwei Kong, Feng Wang, Rui Wu, Mingyu Liang, Niansong Wang, Ling Wang, Guangyuan Zhang, Zeyuan Lu |
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Jazyk: | angličtina |
Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Male Necrosis medicine.medical_treatment Interleukin-1beta 030232 urology & nephrology Nitric Oxide Synthase Type II urologic and male genital diseases Kidney Nephrectomy Rats Sprague-Dawley 0302 clinical medicine biology Anticoagulant Antithrombin Acute kidney injury Acute Kidney Injury female genital diseases and pregnancy complications Nitric oxide synthase Reperfusion Injury Disease Progression Molecular Medicine Original Article medicine.symptom medicine.drug Signal Transduction medicine.medical_specialty medicine.drug_class Antithrombin III Inflammation Collagen Type I 03 medical and health sciences Internal medicine medicine Animals business.industry urogenital system Tumor Necrosis Factor-alpha Macrophages Cell Biology Original Articles medicine.disease Fibrosis Actins Fibronectins Rats Disease Models Animal 030104 developmental biology Endocrinology Gene Expression Regulation biology.protein business chronic kidney disease Kidney disease |
Zdroj: | Journal of Cellular and Molecular Medicine |
ISSN: | 1582-4934 1582-1838 |
Popis: | Acute kidney disease (AKI) leads to increased risk of progression to chronic kidney disease (CKD). Antithrombin III (ATIII) is a potent anticoagulant with anti‐inflammatory properties, and we previously reported that insufficiencies of ATIII exacerbated renal ischaemia‐reperfusion injury (IRI) in rats. In this study, we examined the characteristic of AKI‐CKD transition in rats with two distinct AKI models. Based on our observation, left IRI plus right nephrectomy (NX‐IRI) was used to determine whether ATIII had therapeutic effects in preventing CKD progression after AKI. It was observed that NX‐IRI resulted in significant functional and histological damage at 5 weeks after NX‐IRI compared with sham rats, which was mitigated by ATIII administration. Besides, we noticed that ATIII administration significantly reduced NX‐IRI‐induced interstitial fibrosis. Consistently, renal expression of collagen‐1, α‐smooth muscle actin and fibronectin were substantial diminished in ATIII‐administered rats compared with un‐treated NX‐IRI rats. Furthermore, the beneficial effects of ATIII were accompanied with decreased M1‐like macrophage recruitment and down‐regulation of M1‐like macrophage‐dependent pro‐inflammatory cytokines such as tumour necrosis factor α, inducible nitric oxide synthase and interleukin‐1β, indicating that ATIII prevented AKI‐CKD transition via inhibiting inflammation. Overall, ATIII shows potential as a therapeutic strategy for the prevention of CKD progression after AKI. |
Databáze: | OpenAIRE |
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