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Context: Qi‐dan‐dihuang decoction (QDD) has been used to treat diabetic kidney disease (DKD), but the underlying mechanisms are poorly understood. Objective: This study reveals the mechanism by which QDD ameliorates DKD. Materials and Methods: The compounds in QDD were identified by high‐performance liquid chromatography and quadrupole‐time‐of‐flight tandem mass spectrometry (HPLC‐Q‐TOF‐MS). Key targets and signaling pathways were screened through bioinformatics. Nondiabetic Lepr db/m mice were used as control group, while Lepr db/db mice were divided into model group, dapagliflozin group, 1% QDD‐low (QDD‐L), and 2% QDD‐high (QDD‐H) group. After 12 weeks of administration, 24 h urinary protein, serum creatinine, and blood urea nitrogen levels were detected. Kidney tissues damage and fibrosis were evaluated by pathological staining. In addition, 30 mmol/L glucose‐treated HK‐2 and NRK‐52E cells to induce DKD model. Cell activity and migration capacity as well as protein expression levels were evaluated. Results: A total of 46 key target genes were identified. Functional enrichment analyses showed that key target genes were significantly enriched in the phosphatidylinositol 3‐kinase (PI3K)/protein kinase B (AKT) and mitogen‐activated protein kinase (MAPK) signaling pathways. In addition, in vivo and in vitro experiments confirmed that QDD ameliorated renal fibrosis in diabetic mice by resolving inflammation and inhibiting the epithelial‐mesenchymal transition (EMT) via the p38MAPK and AKT‐mammalian target of rapamycin (mTOR) pathways. Discussion and Conclusion: QDD inhibits EMT and the inflammatory response through the p38MAPK and AKT/mTOR signaling pathways, thereby playing a protective role in renal fibrosis in DKD. [ABSTRACT FROM AUTHOR]

The co-existence of dyes, Cr(VI) and high concentration of salt in dyeing wastewater causes serious and complex environmental problems. In this study, a salt-tolerant strain Bacillus circulans BWL1061 was reported to simultaneously remove 50 mg/L methyl orange and 50 mg/L Cr(VI) under the anaerobic condition with 60 g/L NaCl. During the decolorization process, the Cr(VI) reduction occurred preferentially over the dye decolorization due to the dominate utilization of electron by Cr(VI). The analysis of enzyme activities suggested that azoreductase, NADH-DCIP reductase, and laccase were associated with decolorization of methyl orange. A possible degradation pathway was proposed based on the metabolites analysis. The decolorization of methyl orange is involved in the symmetric cleavage of azo bond, which formed N,N-dimethyl p-phenylenediamine and 4-amino sulfonic acid, or the asymmetric cleavage of azo bond, which formed 4-(dimethylamino) phenol and 4-diazenylbenzene sulfonic acid. Phytotoxicity assays showed that strain BWL1061 could decrease the toxicity of methyl orange to Triticum aestivum , Pogostemon cablin and Isatis indigotica Fort during the decolorization process. In this study, Bacillus circulans is reported for the first time that could simultaneously remove azo dyes and Cr (VI) under high salt condition. [ABSTRACT FROM AUTHOR]

Diabetic nephropathy (DN) is one of the most serious complications of diabetes mellitus, for which no effective treatment currently exists. We tested the hypothesis that Qi-dan-di-huang (QDDH) might have therapuetic effects in an experimental rat model of DN. The levels of I kappa KinaseAlpha and Beta, p-p65, p-IκB alpha, TGF-β1 and Alpha-SMA were significantly increased in kidneys in DN. QDDH decoction only partially reversed the increased Ikappa KinaseAlpha/Beta, p-p65, p-IKappaB alpha, TGF-Beta1 and alpha-SMA in the kidneys in DN. However, treatment of diabetic rats with QDDH decoction significantly inhibited the production and release of inflammatory cytokines IL-6, IL-1 beta and TNF-alpha into the serum. QDDH decoction also significantly improved the physiologic and biochemical indicators of DN, reduced glycogen and protein deposition in DN and prevented renal fibrosis. Together, the data show that QDDH decoction exerts a protective effect on kidneys in diabetic rats and reverses the inflammatory milieu of the serum in DN.

Objective: To identify the main active components in Shenbing decoction Ⅲ and their targets and explore the mechanism by which Shenbing decoction Ⅲ alleviates proteinuria in chronic kidney disease (CKD) based on network pharmacology., Methods: The active components of Shenbing decoction Ⅲ and their potential targets, along with the oral bioavailability and drug-like properties of each component were searched in the TCMSP database. The proteinuria-related targets were searched in the GeneCards database. The active component-target network was constructed using Cytoscape software, and the acquired information of the targets from ClueGO was used for enrichment analysis of the gene pathways., Results: A total of 102 active components were identified from Shenbing decoction Ⅲ. These active components acted on 126 targets, among which 69 were related to proteinuria. Enrichment analysis revealed fluid shear stress- and atherosclerosisrelated pathways as the highly significant pathways in proteinuria associated with CKD., Conclusions: We preliminarily validated the prescription of Shenbing decoction Ⅲ and obtained scientific evidence that supported its use for treatment of proteinuria in CKD. The findings in this study provide a theoretical basis for further study of the mechanism of Shenbing decoction Ⅲ in the treatment of proteinuria in CKD.