The present study aimed to analyze the nephroprotective property of violacein obtained from the bacterium, . The nephrotoxicity in the animal model was induced by gentamicin, potassium dichromate, mercuric chloride, and cadmium chloride-induced nephrotoxicity in the Wistar rats was analyzed by measuring the serum creatinine, uric acid, and urea level. The present investigation revealed the nephroprotective property on convoluted proximal tubule (S1 and S2 segments) and the straight proximal tubule (S3 segment). Also, violacein significantly improved the renal function by the renal protective property on S2 segment of proximal tubule from the nephrotoxicity stimulated by mercuric chloride, potassium dichromate, cadmium chloride and gentamicin in animal models. Animal model studies revealed that violacein at 20 and 40 mg/kg p.o improved the renal function and significantly reduced the increased amount of uric acid, creatinine, and blood urea compared to the control.
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http://dx.doi.org/10.1016/j.sjbs.2020.10.004 | DOI Listing |
Cell Commun Signal
January 2025
Centre of Postgraduate Medical Education, Centre of Translation Research, Department of Biochemistry and Molecular Biology, ul. Marymoncka 99/103, Warsaw, 01-813, Poland.
Background: Renal cell cancer (RCC) is the most common and highly malignant subtype of kidney cancer. Mesenchymal stromal cells (MSCs) are components of tumor microenvironment (TME) that influence RCC progression. The impact of RCC-secreted small non-coding RNAs (sncRNAs) on TME is largely underexplored.
View Article and Find Full Text PDFDiabetes
January 2025
Centre de recherche, Centre hospitalier de l'Université de Montréal (CRCHUM) and Département de médecine, Université de Montréal, 900 Saint Denis Street, Montréal, QC Canada H2X 0A9.
The role of the intrarenal renin-angiotensin system (iRAS) in diabetic kidney disease (DKD) progression remains unclear. In this study, we generated mice with renal tubule-specific deletion of angiotensinogen (Agt; RT-Agt-/-) in both Akita and streptozotocin (STZ)-induced mouse model of diabetes. Both Akita RT-Agt-/- and STZ-RT-Agt-/- mice exhibited significant attenuation of glomerular hyperfiltration, urinary albumin/creatinine ratio, glomerulomegaly and tubular injury.
View Article and Find Full Text PDFMol Biol Rep
January 2025
Department of Endocrinology, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, People's Republic of China.
Background: Tubular injury triggered by hyperglycemia is an important pathological characteristic in diabetic nephropathy (DN). Accumulated advanced glycation end products and their precursor methylglyoxal (MGO), contribute to the development of DN. Carnosine has been shown to prevent the development of DN but the underlying mechanism still needs to be studied in depth.
View Article and Find Full Text PDFSci Rep
January 2025
Medical Imaging Center, First Affiliated Hospital, Jiamusi University, Jiamusi, Heilongjiang, China.
Chronic hyperglycemia, a hallmark of diabetes, can trigger inflammatory responses in the kidney, leading to diabetic nephropathy (DN). Follistatin-like protein 1 (FSTL1) has emerged as a potential therapeutic target in various kidney diseases. This study investigated the effect of high glucose on FSTL1 expression and its role in oxidative stress and cellular transdifferentiation injury in HK-2 human proximal tubule epithelial cells, a model of DN.
View Article and Find Full Text PDFRen Fail
December 2025
Department of Endocrinology, East Hospital, Tongji University School of Medicine, Shanghai, People's Republic of China.
Background: Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease. Sodium-glucose cotransporter protein 2 inhibitors (SGLT2i) are antihyperglycemic agents that provide additional renal-protective effects in patients with DKD, independent of their glucose-lowering effects. However, the underlying mechanism remains unclear.
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