ObjectiveAcute kidney injury (AKI) is a critical clinical condition with high mortality, and specific therapeutic drugs are currently lacking. Although Buyang Huanwu Decoction (BYHWD) has shown clinical efficacy against AKI, its underlying mechanisms remain unclear. This study integrated network pharmacology, in vitro experiments, and animal models to systematically elucidate the potential targets and signaling pathways of BYHWD in treating AKI, and to validate its protective effects on hypoxia/reoxygenation (H/R)-induced endothelial cell injury and renal ischemia-reperfusion injury (IRI) in vivo.MethodsActive components and putative targets of BYHWD were screened using network pharmacology, and their intersections with AKI-related disease targets were identified. Protein-protein interaction (PPI) analysis, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, and molecular docking were performed. An in vitro H/R injury model was established using human umbilical vein endothelial cells (HUVECs). Cell counting kit-8 (CCK-8), trypan blue staining, flow cytometry, and Western blot were applied to assess the effects of BYHWD-containing serum on cell proliferation, apoptosis, oxidative stress, and the expression of proteins related to the VEGFRII/PI3K/AKT/FOXO1 pathway. For in vivo validation, a rat model of AKI was established via renal IRI. Rats were randomly divided into sham, IRI model, and BYHWD treatment groups. Renal function was assessed by measuring serum creatinine (SCr) and blood urea nitrogen levels. Renal histopathological changes were evaluated by hematoxylin and eosin (H&E) and Periodic Acid-Schiff staining.ResultsNetwork pharmacology identified 133 active components in BYHWD and 210 overlapping drug-disease targets. PPI analysis revealed hub genes including VEGFA, AKT1, IL6, and TP53. KEGG enrichment analysis highlighted the PI3K-AKT signaling pathway as a central pathway. Molecular docking demonstrated stable binding of luteolin and quercetin to VEGFA. In vitro experiments confirmed that BYHWD-containing serum increased HUVECs viability, inhibited apoptosis, reduced ROS levels, and modulated the protein expression of Bax/Bcl-2, MCP-1, α-SMA, and CD31. Furthermore, BYHWD activated VEGFRII and the downstream PI3K/AKT/FOXO1 pathway. In animal experiments, BYHWD treatment significantly ameliorated renal dysfunction in IRI-induced AKI rats, as evidenced by decreased SCr and BUN levels. Histopathological examination showed that BYHWD attenuated tubular injury, necrosis, and cast formation.ConclusionBYHWD may alleviate H/R-induced endothelial cell injury by suppressing oxidative stress and apoptosis through active components such as luteolin and quercetin, which target key genes including VEGFA and AKT1, thereby activating the PI3K/AKT/FOXO1 signaling pathway. This study provides integrated experimental evidence from network pharmacology, in vitro, and in vivo studies, supporting the use of BYHWD in AKI treatment.

Systemic lupus erythematosus (SLE) is a typical systemic autoimmune disease that manifests as skin rash, arthritis, lymphadenopathy, and multiple organ lesions. Epigenetics, including DNA methylation, histone modification, and non-coding RNA regulation, mainly affect the function and characteristics of cells through the regulation of gene transcription or translation. Increasing evidence indicates that there are a variety of complex epigenetic effects in patients with SLE, which interfere with the differentiation and function of T, and B lymphocytes, monocytes, and neutrophils, and enhance the expression of SLE-associated pathogenic genes. This paper summarizes our currently knowledge regarding pathogenesis of SLE, and introduces current advances in the epigenetic regulation of SLE from three aspects: immune function, inflammatory response, and lupus complications. We propose that epigenetic changes could be used as potential biomarkers and therapeutic targets of SLE.

Background: In recent years, the disease spectrum has been changing with the change of people's lifestyle.In terms of kidney diseases, the incidence of diabetic nephropathy is increasing year by year and has replaced chronic glomerulonephritis as the primary cause of uremia.Therefore, it is important to delay the progression of renal function in patients with diabetic nephropathy to reduce the occurrence of uremia.Objective: To investigate the efficacy of the treatment of diabetic nephropathy (CKD2-4) with the addition and subtraction of Huangqi-Guizhi-Wuwu Decoction.Method: The 100 patients with diabetic nephropathy were divided into two groups to compare the clinical efficacy.The control group was basic treatment + dapagliflozin, and the observation group was treated with Huangqi-Guizhi-Wuwu Decoction to compare the clinical efficacy, traditional Chinese Medicine (TCM) syndrome integral change, creatinine and urinary protein quantification of the two groups.Expected results: Compared with the dapagliflozin, the addition and subtraction of Huangqi-Guizhi-Wuwu Decoction can significantly reduce the glomerular filtration rate, lower proteinuria of diabetic nephropathy (CKD2-4) and delay the progression of diabetic nephropathy.

膜性肾病(MN)是肾内科难治疾病之一,分为原发性膜性肾病(PMN)和继发性膜性肾病(SMN).肾活检显示,MN发生率达到了22％左右.目前尚缺乏对MN的具体诊断,因此有必要进一步探讨其发病机制和生物标记物.本文从免疫异常、遗传因素、环境因素方面探究MN的发病机制.抗磷脂酶A2受体(PLA2R)是甘露糖受体家族的跨膜糖蛋白成员,他在人类肾脏中表达最强烈.尽管抗PLA2R检测MN的特异度基本上是100％,但在一定程度上模糊了PMN和SMN疾病的区别.因此本文除了着重综述PLA2R以外,还综述了其他几种新发现的生物标记物,旨在进一步为临床诊断与治疗提供帮助.

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Inflammation is a type of defense response against tissue damage, and can be mediated by lymphocytes and macrophages. Fibrosis is induced by tissue injury and inflammation, which leads to an increase in fibrous connective tissue in organs and a decrease in organ parenchyma cells, finally leading to organ dysfunction or even failure. The vascular niche is composed of endothelial cells, pericytes, macrophages, and hematopoietic stem cells. It forms a guiding microenvironment for the behavior of adjacent cells, and mainly exists in the microcirculation, including capillaries. When an organ is damaged, the vascular niche regulates inflammation and affects the repair of organ damage in a variety of ways, such as via its angiocrine function and transformation of myofibroblasts. In this paper, the main roles of vascular niche in the process of organ fibrosis and its mechanism of promoting the progress of fibrosis through inflammatory immunoregulation are summarized. It was proposed that the vascular niche should be regarded as a new therapeutic target for organ fibrosis, suggesting that antifibrotic effects could be achieved by regulating macrophages, inhibiting endothelial-mesenchymal transition, interfering with the angiocrine function of endothelial cells, and inhibiting the transformation of pericytes into myofibroblasts, thus providing new ideas for antifibrosis drug research.