The current study investigated the renoprotective effects of stevia, angiotensin-II type 1 receptor (AT) blocker and calcium (Ca) channel blocker in gentamycin-induced nephrotoxicity in rat models. Six groups of male Sprague-Dawley rats of eight weeks old were taken for the experiment: sham control, nephrotoxicity, treatment with amlodipine (4 mg/kg/day); stevia (200 mg/kg/day); losartan (15 mg/kg/day) and valsartan (5 mg/kg/day), accordingly. The blood sample was taken for the assessment of renal and hepatic-functional variables like serum creatinine, blood urea, BUN and SGPT, SGOT, and total serum bilirubin. Hematological parameters were also examined. Histological examination has been done on kidneys and liver. Alterations of the body weight and the organ's weight were documented. Treatment with stevia and valsartan significantly decreased serum creatinine levels. A reduction of liver enzymes, and total serum bilirubin levels were observed in all the treatment groups. Treatment with valsartan and amlodipine, remarkably and stevia, mildly reduced the renal tissue damage, inflammation, and tubular necrosis. However, the present study demonstrated that losartan treatment aggravated kidney damage by increasing protein cast, calcification, tubular necrosis, and injury. This comparison indicated that both stevia and valsartan have beneficial renoprotective effect and valsartan offers a better treatment option in renal damage over losartan.
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http://dx.doi.org/10.1016/j.toxrep.2019.07.003 | DOI Listing |
Cell Signal
January 2025
Department of Endocrinology, The Second Affiliated Hospital of Anhui Medical University, No. 678 Furong Road, Jingkai District, Hefei 230601, Anhui Province, China; Research Center for Translational Medicine, The Second Affiliated Hospital of Anhui Medical University, No. 678 Furong Road, Jingkai District, Hefei 230601, Anhui Province, China. Electronic address:
Diabetic kidney disease (DKD), a microvascular complication of diabetes mellitus, represents a significant clinical challenge. This study investigated the reno-protective effects of dulaglutide, a glucagon-like peptide-1 receptor agonist (GLP-1 RA) widely used in the management of diabetes, and aimed to elucidate its underlying mechanisms. Mice with db/db and db/m genotypes were allocated into four experimental groups and treated with either dulaglutide or a saline control for 10 weeks.
View Article and Find Full Text PDFFoods
January 2025
Center for Converging Humanities, Kyung Hee University, Seoul 02447, Republic of Korea.
Oncostatin M (OSM) plays a crucial role in diverse inflammatory reactions. Although the food bioactive compound naringenin (NAR) exerts various useful effects, including antitussive, anti-inflammatory, hepatoprotective, renoprotective, antiarthritic, antitumor, antioxidant, neuroprotective, antidepressant, antinociceptive, antiatherosclerotic, and antidiabetic effects, the modulatory mechanism of NAR on OSM expression in neutrophils has not been specifically reported. In the current work, we studied whether NAR modulates OSM release in neutrophil-like differentiated (d)HL-60 cells.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Medicine, Faculty of Medicine, University of Malaysia (UM), Kuala Lumpur 59100, Malaysia.
Aims: To assess the renoprotective effects of dulaglutide and identify mechanisms of action in patients with type 2 diabetes and diabetic kidney disease (DKD).
Materials And Methods: Outpatients/ambulant patients at the Department of Endocrinology, Affiliated Hospital of Xuzhou Medical University between October 2021 and July 2023, with type 2 diabetes and DKD, a urinary albumin-to-creatinine ratio (UACR) ≥ 3 mg/mmol and who were receiving hypoglycemic agents were prescribed dulaglutide at a dose rate of 0.75 - 1.
Background: Heart failure with preserved ejection fraction (HFpEF) and chronic kidney disease (CKD) have a strong pathophysiological interrelationship, and their combination worsens prognosis.
Summary: This article briefly reviews the bidirectional epidemiological burden and the pathophysiological interplay between HFpEF and CKD. It also discusses some of the controversial aspects regarding the diagnosis and screening of HFpEF in CKD patients and focuses on the most effective therapeutic approaches to improve symptoms and prognosis in this high-risk population.
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