Shen Qi Wan ameliorates nephritis in chronic kidney disease via AQP1 and DEFB1 regulation

Liu, Yiming; Hong, Xiao; Liu, Liu; Li, Xinyue; Huang, Shuo; Luo, Qihan; Huang, Qiaoyan; Qiu, Jiang; Qiu, Ping; Li, Changyu

doi:10.1016/j.biopha.2023.116027

Cited by 3 publications

(4 citation statements)

References 36 publications

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“…AQP1 plays an important role in the water reabsorption in the proximal tubules [ 11 ]. However, loss of AQP1 has also been associated with increased tubular injury and inflammation [ 12 ]. Our data demonstrated that mRNA expression of AQP1 was not significantly changed throughout the study period ( Figure 4 A).…”

Section: Resultsmentioning

confidence: 99%

“…The downregulation of AQPs in the collecting duct induced by adenine seems to coincide with a simultaneous decrease in AQP1 expression within the proximal tubules. AQP1 has previously been reported to be downregulated after adenine treatment [ 26 ], and low levels of AQP1 were shown to exacerbate renal inflammation and fibrosis in adenine-treated mice [ 12 ]. These studies revealed that the silencing of AQP1 in cultured proximal tubule cells induced a mesenchymal phenotypic switch [ 26 ], while AQP1-KO in mice resulted in reduced kidney function and increased expression of proinflammatory cytokines [ 12 ].…”

Section: Discussionmentioning

confidence: 99%

“…AQP1 has previously been reported to be downregulated after adenine treatment [ 26 ], and low levels of AQP1 were shown to exacerbate renal inflammation and fibrosis in adenine-treated mice [ 12 ]. These studies revealed that the silencing of AQP1 in cultured proximal tubule cells induced a mesenchymal phenotypic switch [ 26 ], while AQP1-KO in mice resulted in reduced kidney function and increased expression of proinflammatory cytokines [ 12 ]. Additionally, previous studies have shown that AQP1-null mice display increased tubular injury compared to wild-type mice following ischemia–reperfusion [ 27 ] and endotoxin-related acute kidney injury [ 28 ], indicating a role of AQP1 in tubular injury and healing.…”

Section: Discussionmentioning

confidence: 99%

“…Collectively, these findings suggest that the loss of AQP1 may trigger proximal tubule injury, thus accelerating the progression of kidney disease as we observed in the adenine-induced CKD model. Nevertheless, a Chinese compound (Shen Qi Wan (SQW)) consisting of eight Chinese herbs can activate AQP1 and β-defensin 1 (DEFB1), leading to a reduction in the inflammatory response after adenine treatment [ 12 ], indicating a potential therapeutic option of restoring AQP1 expression in CKD.…”

Section: Discussionmentioning

confidence: 99%

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Recovery of Water Homeostasis in Adenine-Induced Kidney Disease Is Mediated by Increased AQP2 Membrane Targeting

Atay,

Elsborg,

Palmfeldt

et al. 2024

IJMS

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Chronic kidney disease (CKD) represents a major public health burden with increasing prevalence. Current therapies focus on delaying CKD progression, underscoring the need for innovative treatments. This necessitates animal models that accurately reflect human kidney pathologies, particularly for studying potential reversibility and regenerative mechanisms, which are often hindered by the progressive and irreversible nature of most CKD models. In this study, CKD was induced in mice using a 0.2% adenine-enriched diet for 4 weeks, followed by a recovery period of 1 or 2 weeks. The aim was to characterize the impact of adenine feeding on kidney function and injury as well as water and salt homeostasis throughout disease progression and recovery. The adenine diet induced CKD is characterized by impaired renal function, tubular injury, inflammation, and fibrosis. A significant decrease in urine osmolality, coupled with diminished aquaporin-2 (AQP2) expression and membrane targeting, was observed after adenine treatment. Intriguingly, these parameters exhibited a substantial increase after a two-week recovery period. Despite these functional improvements, only partial reversal of inflammation, tubular damage, and fibrosis were observed after the recovery period, indicating that the inclusion of the molecular and structural parameters is needed for a more complete monitoring of kidney status.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Recovery of Water Homeostasis in Adenine-Induced Kidney Disease Is Mediated by Increased AQP2 Membrane Targeting

Atay,

Elsborg,

Palmfeldt

et al. 2024

IJMS

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Identification of novel prognostic targets in acute kidney injury using bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2024

Preprint

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Acute kidney injury (AKI) is a type of renal disease occurs frequently in hospitalized patients, which may cause abnormal renal function and structure with increase in serum creatinine level with or without reduced urine output. With the incidence of AKI is increasing. However, the molecular mechanisms of AKI have not been elucidated. It is significant to further explore the molecular mechanisms of AKI. We downloaded the GSE139061 next generation sequencing (NGS) dataset from the Gene Expression Omnibus (GEO) database. Limma R bioconductor package was used to screen the differentially expressed genes (DEGs). Then, the enrichment analysis of DEGs in Gene Ontology (GO) function and REACTOME pathways was analyzed by g:Profiler. Next, the protein-protein interaction (PPI) network and modules was constructed and analyzed, and the hub genes were identified. Next, the miRNA-hub gene regulatory network and TF-hub gene regulatory network were built. We also validated the identified hub genes via receiver operating characteristic (ROC) curve analysis. Overall, 956 DEGs were identified, including 478 up regulated and 478 down regulated genes. The enrichment functions and pathways of DEGs involve primary metabolic process, small molecule metabolic process, striated muscle contraction and metabolism. Topological analysis of the PPI network and module revealed that hub genes, including PPP1CC, RPS2, MDFI, BMI1, RPL23A, VCAM1, ALB, SNCA, DPP4 and RPL26L1, might be involved in the development of AKI. miRNA-hub gene and TF-hub gene regulatory networks revealed that miRNAs and TFs including hsa-mir-510-3p, hsa-mir-6086 and mir-146a-5p, MAX and PAX2, might be involved in the development of AKI. Various known and newtherapeutic targets were obtained via network analysis. The results of the current investigation might be beneficial for the diagnosis and treatment of AKI.

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MRI Scans for Deep Learning-Based Chronic Nephropathy Detection: A Comparison of CNN, MobileNet, VGG16, and ResNet-50 Models

Amanatulla,

Swathi,

Pallavi

et al. 2024

2024 5th International Conference for Emerging Technology (INCET)

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Shen Qi Wan ameliorates nephritis in chronic kidney disease via AQP1 and DEFB1 regulation

Cited by 3 publications

References 36 publications

Recovery of Water Homeostasis in Adenine-Induced Kidney Disease Is Mediated by Increased AQP2 Membrane Targeting

Recovery of Water Homeostasis in Adenine-Induced Kidney Disease Is Mediated by Increased AQP2 Membrane Targeting

Identification of novel prognostic targets in acute kidney injury using bioinformatics and next generation sequencing data analysis

MRI Scans for Deep Learning-Based Chronic Nephropathy Detection: A Comparison of CNN, MobileNet, VGG16, and ResNet-50 Models

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