ABSTRACT
Objective:To assess the effect of rosiglitazone on inflammation in peritoneal dialysis patients. Methods:Fifty patients undergoing continuous ambulatory peritoneal dialysis were collected in our hospital. The treatment group was assigned to receive regular peritoneal dialysis and rosiglitazone 4mg once daily while the control group was received regular peritoneal dialysis for 12 weeks. Such serum examinations as fasting blood glucose (FBG), glycosylated hemoglobin A1c, haemoglobin, serum total cholesterol, high density lipoprotein cholesterol(HDL-C), low density lipoprotein cholesterol, triglycerides and high sensitivity C reactive protein (hs-CRP) were measured, tumor necrosis factorα(TNF-α) and interleukin-6 (IL-6) levels were measured by ELISA, and homeostasis model as-sessment of insulin resistance( HOMA-IR) was also evaluated before and after the treatment. Results:After the 12-week treatment by rosiglitazone, the levels of FPG, HOMA-IR, hs-CRP, TNF-αand IL-6 were declined significantly(P<0. 05), and the level of HDL-C was increased significantly(P<0. 05). Conclusion: Rosiglitazone shows significant anti-inflammatory, insulin resistance improve-ment and anti-lipidemic effects in peritoneal dialysis patients.
ABSTRACT
Radiotherapy is one of the main means of local treatment of breast cancer. Triple negative breast cancer (TNBC) as a molecular subtypes of breast cancer, its biological behavior is special and existing multiple molecular targets, these molecular targets inlfuence the response of ionization radiation through different mechanisms and regulate radiotherapy sensitivity of TNBC This article reviewed the recent advances in radiotherapy and radiosensitivity related molecular targets of TNBC.
ABSTRACT
ObjectiveTo investigate the effects of losartan on angiotensin (Ang)Ⅱ-induced the generation of oxidative stress and expression of transforming growth factor β1(TGF-β1) in rat proximal tubular epithelial cells and to explore its underlying mechanism. MethodsNRK-52E cells, a rat proximal tubular epithelial cell line, were applied to explore the antioxidationand antifibrosis of losartan. The expression of three subunits of nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase, including p47phox, Nox-4, p22phox, and TGF-β1 were determined by real-time RT-PCR and/or Western blot. The generation of reactive oxygen species (ROS) was measured by DCF fluorescence analysis. Superoxide dismutase (SOD) in the supernatant was measured by colorimetric method. Results10-7 mol/L Ang Ⅱ up-regulated p22prox, p47phox and Nox-4 mRNA and protein expression, and the mRNA increased by 5.57-fold, 5.55-fold and 9.41-fold at 24 h (P<0.01, respectively) and the protein increased by 4.53-fold, 4.17-fold and 6.50-fold at 24 h (P<0.01, respectively) as compared with control. Losartan greatly reduced the mRNA elevation of p22prox, p47phox and Nox-4 by 2.71-fold, 2.18-fold and 5.23-fold (P<0.01, respectively) and reduced the protein elevation by 3.20-fold, 2.30-fold and 4.30-fold (P<0.01, respectively) as compared with control. Losartan also inhibited ROS generation induced by Ang Ⅱ in rat proximal tubular epithelial cells. SOD level in the supernatant was markedly decreased after Ang Ⅱ stimulation, while losartan could increase SOD levels (P<0.01). Furthermore, losartan signficantly inhibited Ang Ⅱ-induced TGF-β1 mRNA up-regulation by 64% (P<0.01). ConclusionsLosartan acts as an anti-oxidative and anti-fibrotic agent via the mechanisms of blocking NADPH oxidase-dependent oxidative stress and inhibiting TGF-β1 expression.