The biomechanistic aspects of renal cortical injury induced by diesel exhaust particles in rats and the renoprotective contribution of quercetin pretreatment: Histological and biochemical study

槲皮素 氧化应激 化学 自噬 炎症 ATG5型 药理学 肾皮质 内科学 内分泌学 生物 生物化学 免疫学 医学 抗氧化剂 细胞凋亡
作者
Ahmed A. Morsi,Hanan Fouad,Wardah Abdullah Alasmari,Eman Mohamed Faruk
出处
期刊:Environmental Toxicology [Wiley]
卷期号:37 (2): 310-321 被引量:8
标识
DOI:10.1002/tox.23399
摘要

Abstract Although several studies have reported a toxic effect of diesel exhaust particles (DEP) exposure on the kidney tissues, the involvement of autophagy/NF‐kB signaling as encountered mechanisms and the protective effects of a natural flavonoid, quercetin on DEP remains unclear. Thirty‐two albino rats were divided as control, quercetin‐treated (60 mg/kg, oral), DEP‐exposed (0.5 mg/kg, intra‐tracheal), and quercetin/DEP‐exposed groups. Specimens of the renal cortex were subjected to histo‐biochemical study and immunohistochemical analysis using anti‐NF‐kB, and anti‐LC3β antibodies followed by morphometric and statistical analyses. The expression level of autophagy genes was quantitatively evaluated using RT‐PCR, as well. The DEP‐exposed rats showed an elevation in the renal tissue levels of MDA and a decrease in the catalase and superoxide dismutase (p < .05). Histologically, there were cytoplasmic vacuolar changes in the lining cells of the renal tubules, glomerular atrophy, and vascular congestion. In addition, renal inflammation was evident as confirmed by the increased NF‐kB immunoexpression. Moreover, the gene expression of Becn1, ATG5, and LC3β increased (p <. 0) due to DEP exposure. Conversely, quercetin pretreatment improved these renal histo‐biochemical alterations (p < .05) and regulated autophagy/NF‐kB pathways. Overall, the study proved the renal toxicity mediated by DEP exposure via precipitating renal inflammation, autophagy activation, and oxidative stress. Quercetin pretreatment could antagonize such machinery to protect the kidney against DEP.

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