Browsing by Author "Parada, Belmiro"
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- Effects of Sitagliptin Treatment on Dysmetabolism, Inflammation, and Oxidative Stress in an Animal Model of Type 2 Diabetes (ZDF Rat)Publication . Ferreira, Liliana; Teixeira-de-Lemos, Edite; Pinto, Filipa; Parada, Belmiro; Mega, Cristina; Vala, Helena; Pinto, Rui; Garrido, Patrícia; Sereno, José; Fernandes, Rosa; Santos, Paulo; Velada, Isabel; Melo, Andreia; Nunes, Sara; Teixeira, Frederico; Reis, FlávioThe purpose of this paper is to evaluate the chronic effect of sitagliptin on metabolic profile, inflammation, and redox status in the Zucker Diabetic Fatty (ZDF) rat, an animal model of obese type 2 diabetes. Diabetic and obese ZDF (fa/fa) rats and their controls (ZDF +/+) were treated during 6 weeks with vehicle (control) and sitagliptin (10 mg/kg/bw). Glucose, HbA1c, insulin, Total-c, TGs, IL-1beta, TNF-alpha, CRPhs, and adiponectin were assessed in serum and MDA and TAS in serum, pancreas, and heart. Pancreatic histology was also evaluated. Sitagliptin in diabetic rats promoted a decrease in glucose, HbA1c, Total-c, and TGs accompanied by a partial prevention of insulinopenia, together, with a decrease in CRPhs and IL-1beta. Sitagliptin also showed a positive impact on lipid peroxidation and hypertension prevention. In conclusion, chronic sitagliptin treatment corrected the glycaemic dysmetabolism, hypertriglyceridaemia, inflammation, and hypertension, reduced the severity of the histopathological lesions of pancreatic endocrine and exocrine tissues, together with a favourable redox status, which might be a further advantage in the management of diabetes and its proatherogenic comorbidities.
- Sirolimus ameliorates cyclosporin-induced nephrotoxicity in a rat model – focus on renal lesions, oxidative stress, inflammation, proliferation and angiogenesisPublication . Sereno, José; Romão, Ana M.; Teixeira, Margarida; Parada, Belmiro; Santos, Paulo R.; Alves, Rui; Mega, Cristina; Vala, Helena; Lemos, Edite T.; Teixeira, Frederico; Reis, FlávioSirolimus (SRL) have been pointed as a feasible option for minimize the use of cyclosporine A (CsA), especially because os putatively less nephrotoxicity. However, the cellular mechanism underlying the renoprotection remains to be elucidated, and the clinical data is yet insufficient. This stuty aimed to characterize the histological lesions and the molecular pathways implicated in CsA-induced nephropathy and prevention when converted to SRL.
