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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Apoptosis, Atorvastatin, Cytokines, Female, Fibrosis, Heptanoic Acids, Hydronephrosis, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Immunohistochemistry, In Situ Nick-End Labeling, Muscle, Smooth, Proliferating Cell Nuclear Antigen, Pyrroles, Rats, Rats, Sprague-Dawley, Transforming Growth Factor beta1, Ureter, Ureteral Obstruction.
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Does atorvastatin ameliorate tissue damage of obstructed ureter in rats? Context: To investigate the effects of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor on the tissue damage and fibrosis of obstructed ureters, 80 rats were studied. Atorvastatin, a HMG-CoA reductase inhibitor, was administered to 40 rats at the dose of 20 mg/kg per day 1day before unilateral ligation of ureters and every day thereafter. The other rats served as controls. Eight rats from each group were sacrificed for examination on days 7, 14, 21, 28 and 42 after ligation, respectively. The expressions of transforming growth factor-β1 (TGF-β1), Interleukine-1β (IL-1β), Interleukine-6 (IL-6), tumor necrosis factor-alpha (TNF-α), proliferation cell nuclear antigen (PCNA), and the apoptotic cells in the ureteric smooth muscle were examined. Hydroureter and fibrosis of the muscle layer became progressively aggravated in the ligated ureters of the atorvastatin-treated group and control group. The severities of hydroureter and muscle layer fibrosis in the ligated ureters of the treated group were significantly less than in the control group. The atorvastatin administration also decreased the expression of TGF-β1, IL-1β, IL-6, TNF-α, PCNA and the labeling index of apoptotic cells in the smooth muscle layer of ligated ureters in the treated group.
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We concluded that atorvastatin might ameliorate the tissue damage of obstructed ureters, at least partially, via the inhibition on TGF-β1) expression and by diminishing the effects of pro-inflammatory cytokines. Final Decision: yes