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Published on: September 28, 2015
Luteolin attenuates angiotensin II‑induced renal damage in apolipoprotein E‑deficient mice
Ying-Shu Liu1, Qin Yang2, Shen Li1
1Department of Endocrinology, Dalian Municipal Central Hospital Affiliated of Dalian Medical University, Dalian, Liaodong 116011, P.R. China.
Abstract:
Renal damage is a common and severe condition encountered in the clinic. Luteolin (Lut) exhibits anti‑inflammatory, anti‑fibrotic and anti‑apoptotic effects. Thus, the present study aimed to investigate the pharmacological effects of Lut on angiotensin II (AngII)‑induced renal damage in apolipoprotein E‑deficient (ApoE‑/‑) mice. Male ApoE‑/‑ mice (age, 8 weeks) were randomly divided into the following three groups: i) Control group (n=6); ii) AngII group (n=6); and iii) AngII + Lut group (n=6). Lut was administered by gavage (100 mg/kg/d). ApoE‑/‑ mice were implanted with Alzet osmotic minipumps, filled with either saline vehicle or AngII solution for a maximum period of 4 weeks. After 4 weeks, metabolic characteristics were measured and the histopathological alterations in the kidney tissue were observed. The metabolic characteristics of blood creatinine (CRE) levels were lower in the AngII + Lut group compared with in the AngII group. The expression levels of collagen I and III were lower in the kidney tissues of the AngII + Lut group compared with the corresponding tissues of the AngII group. The gene expression levels of IL‑1β, IL‑6, TNF‑α and IL‑10 were also suppressed in the kidney tissues of the AngII + Lut group compared with those in the corresponding tissues of the AngII group. Furthermore, the AngII + Lut group exhibited markedly increased LC3 protein expression and notably decreased p62 protein expression in the kidney tissues compared with the expression levels in the AngII group. The data demonstrated that Lut attenuated AngII‑induced collagen deposition and inflammation, while inducing autophagy. Collectively, the results suggested that Lut treatment exhibited a exerted effect on AngII‑induced renal injury in ApoE‑/‑ mice.
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