THYMOQUINONE PROTECTS AGAINST ANGIOTENSIN II-INDUCED RENAL DAMAGE VIA ANTI-FIBROSIS AND ANTI-INFLAMMATORY EFFECTS IN APOE-DEFICIENT MICE

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Objective: Many studies showed that angiotensin II(Ang II) is a potent biologically active product of renin-angiotensin system and a key regulator of renal inflammation and fibrosis. Thymoquinone (TQ) is an herbal medicine which has been shown to have anti-inflammatory and anti-fibrosis effects in previous our studies. The aim of this study was to determine the role of TQ in Ang II-induced renal damage. Design and method: In present study, we used a model of Ang II-induced renal damage in ApoE-deficient (ApoE−/−) mice. Thirty eight-week-old male ApoE-/- mice were randomly divided into three groups: a control group, Ang II group and Ang II + TQ group. All groups mice were with different treated for 4 weeks. Blood samples were obtained from the inferior vena cava and collected in serum tubes; the blood samples were stored at minus 80°C until use. Coronal sections of kidney tissues were fixed in 10% formalin and then embedded in paraffin for histological evaluation. The kidney was stored in liquid nitrogen for immunoblotting or mRNA analysis. All data are presented as the mean ± SEM. Statistical analysis was performed using SPSS software version 23.0 (SPSS Inc., Chicago, IL, USA). Inter-group variation was measured by one-way ANOVA and subsequent Tukey's test. The minimal level of significance was P < 0.05. Results: The Ang II group showed a marked increase in CRE levels in ApoE-/- mice, but these parameters were significantly decreased in the Ang II + TQ group(Table1). There were significant pathophysiological changes (HE and Masson staining) in Ang II group mice, but the pathophysiological changes were inhibited in Ang II + TQ group(Figure1). Thymoquinone reduced Ang II-induced kidney fibrosis and inflammation in ApoE-/- mice(Figure2 and 3). Conclusions: Our data established that thymoquinone helps mitigate AngII-induced renal damage as shown by the downregulation of fibrosis expression and the suppression of inflammatory markers.