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Objective. To study the efficacy of restricting dietary protein intake combined with Buyang Huanwu decoction in treating diabetic nephropathy (DN) and its effect on patients’ inflammatory factor levels. Methods. The medical data of 150 DN patients treated in Wuhan No.1 Hospital (June 2018—May 2021) were retrospectively analyzed. All patients received regular therapy, those who received the intervention of restricting dietary protein intake were included in the control group (n = 75), and on this basis, those treated with Buyang Huanwu decoction were included in the experimental group (n = 75), so as to scientifically evaluate their efficacy and inflammatory factor levels after treatment. Results. The patients’ general information was not statistically different between the two groups ( P > 0.05 ); after treatment, the experimental group gained remarkably higher marked effective rate and total effective rate of treatment than the control group ( P < 0.05 ); the inflammatory factor levels of all patients were obviously better than before ( P < 0.05 ), and the levels of TNF-α, IL-2, IL-8, IL-4, and IL-10 were obviously lower in the experimental group than in the control group ( P < 0.05 ); the levels of fasting blood glucose, 2 h postprandial blood glucose, and glycosylated hemoglobin of all patients were remarkably lower than before ( P < 0.05 ), but with no significant between-group difference ( P > 0.05 ); the renal function indexes of all patients were better than before, and between the two groups, the levels of 24 h microalbuminuria, 24 h urine protein excretion, and serum creatinine were obviously lower and the glomerular filtration rate was significantly higher in the experimental group ( P all <0.05), and the patients’ traditional Chinese medicine (TCM) symptom scores were remarkably lower in the experimental group ( P < 0.05 ). Conclusion. Jointly applying Buyang Huanwu decoction on the basis of restricting dietary protein intake can effectively promote the clinical efficacy of DN, which is conducive to adjusting the inflammatory factor levels, promoting the patients’ renal function, and alleviating the clinical symptoms.

Background Circular RNA (circRNA) has been shown to mediate diabetic nephropathy (DN) development by regulating renal tubular epithelial cells (RTECs) injury. However, the role and mechanism of circ_0000064 in high glucose (HG)-induced RTECs injury have not been fully elucidated. Methods Human RTECs (HK-2) were exposed to HG to induce cell injury. Cell oxidative stress was assessed by detecting the levels of oxidative stress-markers. Moreover, cell proliferation and apoptosis were determined by CCK8 assay, EDU assay and flow cytometry. The protein levels of proliferation markers, apoptosis markers and Rho-associated coiled-coil-containing kinase 1 (ROCK1) were measured using western blot analysis. Furthermore, quantitative real-time PCR was performed to assess the expression of circ_0000064, microRNA (miR)-532-3p and ROCK1. The interaction between miR-532-3p and circ_0000064 or ROCK1 was confirmed by dual-luciferase reporter assay and RNA pull-down assay. Results Our results revealed that HG treatment could promote HK-2 cells oxidative stress, apoptosis, fibrosis, and inhibit proliferation. Circ_0000064 expression was increased in the serum of DN patients and HG-induced HK-2 cells, and silenced circ_0000064 could relieve HG-induced HK-2 cells injury. MiR-532-3p could be sponged by circ_0000064, and its overexpression also alleviated HG-induced HK-2 cells injury. Besides, the regulation of circ_0000064 knockdown on HG-induced HK-2 cells injury could be reversed by miR-532-3p inhibitor. Additionally, ROCK1 was a target of miR-532-3p, and its expression was inhibited by circ_0000064 knockdown. The inhibition effect of circ_0000064 knockdown on HG-induced HK-2 cells injury also could be reversed by overexpressing ROCK1. Conclusion In summary, circ_0000064 knockdown might alleviate HG-induced HK-2 cells injury via regulating the miR-532-3p/ROCK1 axis, which provided a new perspective for DN treatment.

Oxygen glucose deprivation/re-oxygenation (OGD/R)-mediated ischemia of kidney is frequently leads to enhanced apoptosis and amplified inflammatory response. Sappanchalcone (Sap) is a flavonoid compound that extracted from Caesalpinia sappan L. with a range of cell-protective activities. Herein, we primarily reconnoitered the influence of Sap in HK-2 cells under OGD/R treatment. In this research, the consequence revealed that Sap might linked with ischemia of kidney. Besides, Sap lessened OGD/R-mediated HK-2 cell injury by boosting cell viability, inhibiting apoptosis and inflammation. In addition, Sap hindered activation of the TNFRSF1A/NF-kB signaling. Moreover, upregulation of TNFRSF1A diminished the repressive influence of Sap on OGD/R-mediated apoptosis and inflammation. In conclusion, Sap declined the OGD/R-induced HK-2 cell injury by downregulation of TNFRSF1A/NF-kB signaling, thereby offered a theoretical basis for the handling of ischemia of kidney.