4.7 Article

Ferulic acid ameliorates renal injury via improving autophagy to inhibit inflammation in diabetic nephropathy mice

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BIOMEDICINE & PHARMACOTHERAPY
卷 153, 期 -, 页码 -

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ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2022.113424

关键词

Diabetic nephropathy; Ferulic acid; Autophagy; Inflammation

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This study aimed to investigate the nephroprotective effect of ferulic acid (FA) on diabetic nephropathy (DN) and its underlying mechanism using a mouse model. The results showed that FA reduced body weight and fasting blood glucose levels, improved renal organ coefficient, and decreased protein and nitrogen levels in urine and blood, as well as cholesterol levels in serum. Additionally, FA enhanced autophagy and suppressed inflammation in the renal tissues. These findings suggest that FA plays a positive role in alleviating renal injury in DN mice.
Diabetic nephropathy (DN) is one of the most serious microvascular complications following diabetes mellitus (DM). Ferulic acid (FA), a phenolic acid widely found in plants, has multiple pharmacological effects such as anti-oxidation, anti-inflammation and anti-tumor. However, the current research on FA in the field of DN is insufficient. The present study aimed to explore the nephroprotective effect of FA on DN in mice and reveal its underlying mechanism. DN was induced by high-fat diet (HFD) combined with streptozotocin (STZ) injection in male C57BL/6J mice. Animals were randomly divided into four groups (n = 8): Control group, DN group, FA group (200 mg/kg FA, i.g.) and valsartan (VAL) group (12 mg/kg VAL, i.g.). The drug was administered once a day for 8 weeks. Treated with FA, the body weight and fasting blood glucose (FBG) of DN mice were reduced and the renal organ coefficient was significantly optimized. Meanwhile, FA decreased levels of 24-h urine protein excretion (24-h UP) in urine and blood urea nitrogen (BUN), creatinine (Cr) in serum, reduced levels of triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) in serum. In addition, FA promoted light chain 3 (LC3) expression markedly, and inhibited the expressions of p62, NOD-like receptor family pyrin domain containing 3 (NLRP3) and interleukin-1 beta (IL-1 beta) in renal tissues. In conclusion, FA played a positive role in alleviating renal injury in HFD/STZ-induced DN mice by enhancing autophagy and suppressing excessive inflammation.

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