Abstract:
:This study aimed at evaluating the protective effects of a herbal medication (Tutukon) on the hyperoxaluria induced apoptotic changes and crystal deposition in renal tubular epithelium in rat model. 60 male wistar rats were divided into three different groups (each group n: 20). In Group I severe hyperoxaluria was induced by ethylene glycol (EG) (0.75%) administration for 28 days. In Group II, in addition to hyperoxaluria induction, animals were treated with Tutukon for 28 days. Group III animals constituted the controls without any specific medication and/or intervention. While the presence and degree of crystal deposition in the tubular lumen were examined histopathologically under light microscopy, tubular apoptotic changes were evaluated using immunohistochemical staining for cysteine-aspartic acid protease-3 (Caspase-3) and tumor necrosis factor alpha (TNF-α) positivity on days 14 and 28, respectively. Evaluation of apoptotic changes by Caspase-3 positivity showed that while the majority of animals undergoing EG only showed evident apoptotic changes (n: 9), Tutukon application demonstrated a significant limitation with limited or no apoptosis (n: 7) in these animals. Similar data were noted for TNF alpha expression; while apoptotic changes were evident in 8 (80%) in Group I animals, limited changes were noted in Tutukon Group (n: 2). Regarding crystal deposition despite evident changes in Group I (9 animals), like apoptotic alterations, it was again significantly limited in animals receiving Tutukon (4 animals). Renal tubular crystal deposition and apoptotic changes induced by hyperoxaluria play a role in the pathogenesis of urolithiasis and the limitation of these changes might be instituted by Tutukon as a result of its antioxidant and antiinflammatory effects.
journal_name
Urolithiasisjournal_title
Urolithiasisauthors
Sahin C,Sarikaya S,Basak K,Cetinel CA,Narter F,Eryildirim B,Saglam E,Sarica Kdoi
10.1007/s00240-015-0777-1subject
Has Abstractpub_date
2015-08-01 00:00:00pages
313-22issue
4eissn
2194-7228issn
2194-7236journal_volume
43pub_type
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