Abstract：Objective: To investigate the effects of benzo[b]fluoranthene (BbF) intervention on renal inflammation and the advanced glycation end products/receptor for advanced glycation end products (AGE/RAGE) signaling pathway in rats with chronic kidney disease (CKD). Methods: A total of 53 specific pathogen-free (SPF) male Sprague-Dawley (SD) rats were used. Fourteen rats were randomly selected as the control group, and the remaining 39 rats were used to establish a CKD model. Among them, 36 rats were successfully modeled and randomly divided into three groups: the model group (14 rats), the BbF group (11 rats), and the BbF + FPS-ZM1 group (11 rats). The body weight changes of rats in each group were compared before and after gavage. After 4 weeks of gavage, a balance was used to measure the weight of both kidneys and the kidney index; hematoxylin-eosin (HE) staining was used to detect pathological changes in renal tissue. Tail vein blood was collected after 4 weeks of gavage, and a biochemical analyzer was used to detect renal function indicators [serum creatinine (Scr), blood urea nitrogen (BUN), uric acid (UA)]. Renal tissue was collected after 4 weeks of gavage; enzyme-linked immunosorbent assay (ELISA) was used to detect the content of inflammatory factors [C-reactive protein (CRP), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α)] and the levels of oxidative stress [superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px)]; flow cytometry was used to detect the expression levels of macrophage-related markers [CD11c+, CD206+, CD11c+/CD206+]; Western blotting (Wb) was used to detect the levels of the AGE/RAGE signaling pathway. Results: With the extension of gavage time, the body weight of rats in the control group showed a gradual increase trend, while the body weight of rats in the model group, BbF group, and BbF + FPS-ZM1 group all showed a decreasing trend, with a significant decrease in the BbF group (P<0.05). In addition, the pathological changes in the BbF group were obvious. Compared with the control group, model group, and BbF+FPS-ZM1 group, the BbF group had significantly increased levels of kidney weight, kidney index, UA, BUN, Scr, IL-6, CRP, TNF-α, IL-8, MDA, CD11c+/CD206+, CD11c+, RAGE mRNA, and AGE mRNA, while the levels of GSH-Px, SOD, and CD206+ were significantly decreased, with statistically significant differences (P<0.05). Conclusion: BbF can promote the development of inflammation in CKD rats, accelerate the progression of the disease by activating the AGE/RAGE signaling pathway, and at the same time have adverse effects on oxidative stress, renal function, and macrophages.
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2025, Vol. 31 
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