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
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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