The correlation between dietary inflammatory index and risk of hyperuricemia in the U.S. population.

The dietary inflammatory index (DII) has been reported to be related to chronic diseases as a novel inflammatory marker. However, the correlation between DII score and hyperuricemia in adults in the United States is still unclear. Therefore, our goal was to explore the correlation between them. A total of 19,004 adults were enrolled in the National Health and Nutrition Examination Survey from 2011 to 2018. DII score was calculated according to 28 dietary items obtained by 24-hour dietary interview data. Hyperuricemia was defined by serum uric acid level. We used multilevel logistic regression models and subgroup analysis to determine whether the 2 were associated. DII scores were positively associated with serum uric acid and the risk of hyperuricemia. Per unit increased in DII score was associated with a 3 mmol/L increase in serum uric acid in males (ß 3.00, 95% confidence interval (CI) 2.05-3.94) and 0.92mmol/L in females (ß 0.92, 95% CI 0.07-1.77), respectively. Compared with the lowest tertile of DII score, the rise of DII grade increased the risk of hyperuricemia among the whole participants (T2: odds ratio (OR) 1.14, 95% CI 1.03, 1.27; T3: OR 1.20 [1.07, 1.34], P for trend = .0012) and males [T2: 1.15 (0.99, 1.33), T3: 1.29 (1.11, 1.50), P for trend = .0008]. For females, the correlation between DII score and hyperuricemia was statistically significant in the subgroup stratified by body mass index (BMI) (BMI < 30, OR 1.08, 95% CI 1.02-1.14, P for interaction = .0134), which indicates that the association depends on BMI. In the United States male population, the DII score has a positive correlation with hyperuricemia. Anti-inflammatory dietary intake can be beneficial for lower serum uric acid.

Sanqi Qushi Granule Alleviates Proteinuria and Podocyte Damage in NS Rat: A Network Pharmacology Study and in vivo Experimental Validation.

Background: Nephrotic syndrome (NS) and its numerous complications remain the leading causes of morbidity and mortality globally. Sanqi Qushi granule (SQG) is clinically effective in NS. However, its potential mechanisms have yet to be elucidated. Methods: A network pharmacology approach was employed in this study. Based on oral bioavailability and drug-likeness, potential active ingredients were picked out. After acquiring overlapping targets for drug genes and disease-related genes, a component-target-disease network and protein-protein interaction analysis (PPI) were constructed using Cytoscape, followed by GO and KEGG enrichment analyses. Adriamycin was injected into adult male Sprague-Dawley (SD) rats via the tail vein to establish NS model. Kidney histology, 24-hr urinary protein level, creatinine (Cr), blood urea nitrogen (BUN), triglyceride (TG), total cholesterol (TC), and low-density lipoprotein (LDL-C) level were assessed. Western blotting, immunohistochemistry, and TUNEL staining were applied. Results: In total, 144 latent targets in SQG acting on NS were screened by a network pharmacology study, containing AKT, Bax, and Bcl-2. KEGG enrichment analysis suggested that PI3K/AKT pathway was enriched primarily. In vivo validation results revealed that SQG intervention ameliorated urine protein level and podocyte lesions in the NS model. Moreover, SQG therapy significantly inhibited renal cells apoptosis and decreased the ratio of Bax/Bcl-2 protein expression. Moreover, we found that Caspase-3 regulated the PI3K/AKT pathway in NS rats, which mediated the anti-apoptosis effect. Conclusion: By combining network pharmacology with experimental verification in vivo, this work confirmed the treatment efficacy of SQG for NS. SQG protected podocyte from injury and inhibited kidney apoptosis in NS rats via the PI3K/AKT pathway at least partially.