Renal tubular epithelial cell (TEC) injury and fibrosis are the key factors of the pathogenesis of chronic kidney disease. Here, we reported that tectorigenin is effectively protected against obstructive nephropathy established by unilateral ureteral obstruction (UUO). In vivo, tectorigenin administration significantly alleviated the deteriorations of renal functions including blood urea nitrogen and creatinine. Meanwhile, results from the histology suggested that renal injury characterized by tubular cell damage and fibrosis lesions of kidneys in UUO group were markedly attenuated following tectorigenin treatment. Mechanistically, we found that tectorigenin treatment greatly inhibited Smad3 phosphorylation, and the transcription and protein level of Nox4, a newly identified direct downstream molecule of Smad3 and a modulator of ferroptosis, while it indirectly restored the expression of glutathione peroxidase 4, a negative regulator of ferroptosis. Consistent with in vivo studies, treatment with tectorigenin also suppressed the ferroptosis induced by erastin/RSL3 and fibrosis stimulated by transforming growth factor β1 (TGF‐β1) in primary renal TECs. What is more, treatment with ferroptosis inhibitor, ferrostatin‐1, also impeded TGF‐β1 stimulated the profibrotic effects in TECs, indicating that tectorigenin may relieve fibrosis by inhibiting ferroptosis in TECs. In addition, tectorigenin treatment exhibited a similar tendency, which inhibited Smad3 activation, and the docking analysis revealed that tectorigenin docked well into the Smad3 binding cavity with strong binding affinity (−7.9 kcal/mol). Thus, this study deciphers the protective effect of tectorigenin against obstructive nephropathy through inhibiting Smad3‐mediated ferroptosis and fibrosis.

Aim: Aldosterone is elevated in many diseases such as hypertension, diabetic nephropathy and chronic kidney disease, etc. The aim of this study was to investigate the effects of aldosterone on intracellular ROS production and autophagy in podocytes in vitro, and to explore the possibility of ginsenoside Rg1 (Rg1) being used for protecting podocytes from aldosterone-induced injury. Methods: MPC5 mouse podocyte cells were tested. Autophagosome and autophagic vacuole formation were examined under confocal microscopy with MDC and acridine orange staining, respectively. ROS were detected with flow cytometry. Malondialdehyde content and superoxide dismutase (T-SOD) activity were measured using commercial kits. The expression of LC3-II, beclin-1, SOD2 and catalase was measured by Western blotting. Results: Treatment with aldosterone (10 nmol/L) significantly increased ROS generation and the expression of SOD2 and catalase in MPC5 cells. Furthermore, treatment with aldosterone significantly increased the conversion of LC3-I to LC3-II, beclin-1 expression and autophagosome formation. Co-treatment with rapamycin (1 ng/mL) or chloroquine (10 μmol/L) further increased aldosterone-induced autophagosome formation. Co-treatment with Rg1 (80 ng/mL) effectively relieved oxidative stress and increased T-SOD activity at the early stage and subsequently decreased autophagy in aldosterone-treated podocytes. Co-treatment with 3-MA (4 mmol/L) or NAC (50 mmol/L) exerted similar effects against aldosterone-induced autophagy in podocytes. Conclusion: Aldosterone enhances ROS generation and promotes autophagy in podocytes in vitro. Ginsenoside-Rg1 effectively relieves aldosterone-induced oxidative stress, thereby indirectly inhibiting aldosterone-induced podocyte autophagy.

Objective In this case–control study, we retrospectively analyzed the intestinal flora compositions of patients with early-stage chronic kidney disease (CKD). Methods Forty-seven patients with early CKD who were treated at the Traditional Chinese Medicine Hospital between March and October 2018 were enrolled, and 150 healthy volunteers were enrolled in the healthy control group. Fresh stool samples were collected. The V3–V4 region of the bacterial 16S rRNA was amplified via PCR. Biterminal sequencing was performed using the Illumina MiSeq platform. The flora compositions were compared between the two groups. Results The Chao1 and Shannon indices showed significantly lower intestinal flora diversity and abundances in the CKD group than in the healthy controls. Beta diversity analysis revealed notable differences in the intestinal flora compositions between the groups. At the phylum level, Actinobacteria and Proteobacteria abundances were significantly higher in the CKD group. Thirty-one species differed significantly between both groups, among which, differences in Ruminococcus and Roseburia displayed the highest diagnostic values for distinguishing CKD patients from healthy controls. Conclusions Intestinal flora compositions are altered in early-stage CKD patients among the Han population in southwestern China.

Systemic lupus erythematosus (SLE) is a common autoimmune disease, which features the secretion of antibodies directed against autoantigens in vivo. In the present study, a peptide microarray was developed to detect the epitopes recognized by autoantibodies in patients with SLE for an effective method of diagnosis. SLE-associated epitopes in 14 autoantigens were predicted using the antigenic epitope prediction software DNA star. Peptides were synthesized based on the predicted antigenic epitopes and immobilized on a slide surface and developed into a peptide microarray. Using this peptide microarray the autoantibodies in 120 patients with SLE and 110 healthy subjects were detected. A total of 73 potential antigenic epitopes in 14 autoantigens were predicted and screened. The peptide microarray based on the 73 epitopes was used to detect the autoantibodies in patients with SLE. A total of 14 epitopes with potential diagnostic values were screened out. The sensitivity and specificity of the 14 epitopes for the diagnosis of SLE were 71.6 and 85.8%, respectively. An optimal set of epitopes for SLE diagnosis was obtained. As individual patients had a specific autoantibody spectrum it was possible to detect autoantibodies in SLE and perform the diagnosis of SLE using the peptide microarray.