Life sciences · 2011
Atorvastatin ameliorates tissue damage of obstructed ureter in rats.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Chuang Yen-Hwang, Chuang Wan-Long, Huang Shu-Pin, Liu Ching-Kuan, Huang Chun-Hsiung
Аннотация
AIMS: 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.
MAIN METHODS: 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.
KEY FINDINGS: 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.
SIGNIFICANCE: 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.
MAIN METHODS: 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.
KEY FINDINGS: 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.
SIGNIFICANCE: 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.
Предметные рубрики MeSH
AnimalsApoptosisAtorvastatinCytokinesFemaleFibrosisHeptanoic AcidsHydronephrosisHydroxymethylglutaryl-CoA Reductase InhibitorsImmunohistochemistryIn Situ Nick-End LabelingMuscle, SmoothProliferating Cell Nuclear AntigenPyrrolesRatsRats, Sprague-DawleyTransforming Growth Factor beta1UreterUreteral Obstruction