The objective of this study is to investigate if sinomenine hydrochloride (SIN-HCl) could be effective against adriamycin-induced renal fibrosis by regulating autophagy in a rat model. Forty male Sprague-Dawley (SD) rats were randomly divided into control group, model group, telmisartan group, and SIN-HCl group; rat model was induced by adriamycin; all rats were given intragastric administration for 6 weeks. Urine was collected from rats in metabolic cages to determine 24 h protein level. This was done after intragastric administration for the first two weeks and then once for every two weeks. Renal pathological changes were examined by the staining of HE, Masson, and PASM. Expressions and distributions of fibronectin (FN), laminin (LN), light chain 3 (LC3), and Beclin-1 were observed by immunohistochemistry. SIN-HCl ameliorates proteinuria, meanwhile attenuating the renal pathological changes in adriamycin-induced rats and also attenuating renal fibrosis and excessive autophagy by reducing the expression of FN, LN, LC3, and Beclin-1. SIN-HCl attenuates renal fibrosis by inhibiting excessive autophagy induced by adriamycin and upregulates the basal autophagy.
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http://dx.doi.org/10.1155/2017/6878795 | DOI Listing |
Cardiol Rev
January 2025
From the First Department of Cardiology, School of Medicine, National and Kapodistrian University of Athens, Hippokration General Hospital, Athens, Greece.
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School of Veterinary Medicine, College of Bio-Resources and Agriculture, Institute of Veterinary Clinical Science, National Taiwan University, Taipei, Taiwan.
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View Article and Find Full Text PDFMol Ther
January 2025
Department of Nephrology, First Medical Center of Chinese PLA General Hospital, National Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Diseases Research, Beijing, 100853, China. Electronic address:
Acute kidney injury (AKI) can progress to chronic kidney disease (CKD) and subsequently to renal fibrosis. Poor repair of renal tubular epithelial cells (TECs) after injury is the main cause of renal fibrosis. Studies have shown that restoring damaged fatty acid β-oxidation (FAO) can reduce renal fibrosis.
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View Article and Find Full Text PDFInt J Biol Sci
January 2025
Department of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Kidney stone disease is a major risk factor for impaired renal function, leading to renal fibrosis and end-stage renal disease. High global prevalence and recurrence rate pose a significant threat to human health and healthcare resources. Investigating the mechanisms of kidney stone-induced injury is crucial.
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