Propylthiouracil modulates aortic vasculopathy in the oxidative stress model of systemic sclerosis |
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| Affiliation: | 1. Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy;2. Division of Rheumatology, Department of Internal Medicine, University of Louisville, Louisville, KY, USA;3. Department of Paediatric, Gynaecological, Microbiological and Biomedical Sciences, University of Messina, Messina, Italy;1. Department of Plastic and Reconstructive Surgery, Nanfang Hospital, Southern Medical University, Guangzhou 510515, Guangdong, China;2. Department of Breast Surgery, Guangdong Traditional Chinese Medicine Hospital, Guangzhou 510000, Guangdong, China;3. Department of Plastic Surgery, The Third Affiliated Hospital of Guangzhou Medical College, Guangzhou 510150, Guangdong, China;4. Department of Pathology, Guangdong Traditional Chinese Medicine Hospital, Guangzhou 510000, Guangdong, China;1. Department of Molecular and Cellular Sports Medicine, German Sport University Cologne, Cologne, Germany;2. The German Research Centre of Elite Sport, German Sport University Cologne, Cologne, Germany;3. Olympic Training Centre Rhineland, Cologne, Germany;4. Division of Physical Activity, Prevention and Cancer, National Center for Tumor Diseases (NCT) and German Cancer Research Center, Heidelberg, Germany |
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| Abstract: | BackgroundIn systemic sclerosis (SSc) vasculopathy affects small arteries and capillaries, but recent evidences show also macrovascular alterations. Experimental data suggest that propylthiouracil (PTU) abrogates the development of cutaneous and pulmonary fibrosis during SSc. The aim of this study was to evaluate the effect of propylthiouracil on aortic lipid peroxidation, intima-media thickness and myofibroblasts differentiation in experimental SSc.MethodsSSc was induced in BALB/c mice by daily subcutaneous injections of hypochlorous acid (HOCl) for 6 weeks. Mice (n = 25) were randomized to receive daily: HOCl (n = 10), HOCl + PTU (n = 10), or vehicle (n = 5). Thoracic aorta was evaluated by histological methods to measure intima-media thickness and by immunostaining for α-smooth muscle actin (α-SMA) to assess myofibroblast differentiation. Aortic and plasma levels of malondialdehyde (MDA) were also measured.ResultsHOCl induced a significant increase in aortic intima-media thickness compared to controls (p < 0.001), while PTU administration prevented intima-media thickening (p < 0.01). Myofibroblast differentiation was also less evident in HOCl + PTU-treated animals (p < 0.05) compared to mice treated with HOCl alone. The increase in aortic and plasma MDA levels induced by HOCl, was significantly prevented by PTU administration (p < 0.05).ConclusionPTU, by reducing lipid peroxidation, prevents aortic thickening and myofibroblast differentiation induced by HOCl, reducing macrovascular alterations in experimental SSc. |
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