LLLT caused significant changes in inflammatory biomarkers and oxidative stress: decreased levels of fibrinogen, L-citrulline and SOD as opposed to the increase of NO in rats with experimental myopathies and significant muscle recovery.

Fiore MC, Jimenez PM, Cremonezzi D, Juncos LI, García NH. Statins reverse renal inflammation and endothelial dysfunction induced by chronic high salt intake. Am J Physiol Renal Physiol 301: F263-F270, 2011. First published May 4, 2011 doi:10.1152/ajprenal.00109.2010.-High salt intake (HS) is a risk factor for cardiovascular and kidney disease. Indeed, HS may promote blood-pressure-independent tissue injury via inflammatory factors. The lipid-lowering 3-hydroxy 3-methylglutaryl-coenzyme A (HMGCoA) reductase inhibitors exert beneficial lipid-independent effects, reducing the expression and synthesis of inflammatory factors. We hypothesized that HS impairs kidney structure and function in the absence of hypertension, and these changes are reversed by atorvastatin. Four groups of rats were treated for 6 wk in metabolic cages with their diets: normal salt (NS); HS, NS plus atorvastatin and HS plus atorvastatin. We measured basal and final body weight, urinary sodium and protein excretion (UProtV), and systolic blood pressure (SBP). At the end of the experimental period, cholesterolemia, creatinine clearance, renal vascular reactivity, glomerular volume, cortical and glomerular endothelial nitric oxide synthase (eNOS), and transforming growth factor (TGF)-␤1 expression were measured. We found no differences in SBP, body weight, and cholesterolemia. HS rats had increased creatinine clearence, UProtV, and glomerular volume at the end of the study. Acetylcholine-induced vasodilatation decreased by 40.4% in HS rats (P Ͻ 0.05). HS decreased cortical and glomerular eNOS and caused mild glomerular sclerosis, interstitial mononuclear cell infiltration, and increased cortical expression of TGF-␤1. All of these salt-induced changes were reversed by atorvastatin. We conclude that long-term HS induces inflammatory and hemodynamic changes in the kidney that are independent of SBP. Atorvastatin corrected all, suggesting that the nitric oxide-oxidative stress balance plays a significant role in the earlier stages of salt induced kidney damage.atrovastatin; blood pressure; kidney injury HIGH SALT (sodium chloride) intake, an established habit in industrialized nations, is an important risk factor for cardiovascular (27) and kidney disease (42). Indeed, clinical and experimental studies have shown an independent association between increased dietary salt intake and left ventricular hypertrophy, urine protein excretion, and renal fibrosis and disease progression (9, 23). These associations could be of great significance as proteinuria and renal disease have been implicated as independent risk factors for cardiovascular mortality in hypertensive and diabetic patients and in the elderly (18).Although a high-salt (HS) diet increases blood pressure in susceptible humans and in experimental animals (19,34,40), it can also cause tissue injury independently of blood pressure. For instance, salt promotes kidney and myocardial fibrosis along with increased transforming growth factor (TGF)-␤ 1 expression and abnormal microvascular function, all...

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Chagas infection is a major endemic disease affecting Latin American countries. The persistence of Trypanosoma cruzi generates a chronic inflammatory reactivity that induces an immune response directed to the host's tissues. The effectiveness of the treatment in the chronic phase is still unsatisfactory due, amongst other reasons, to the collateral effects of the drugs used. We investigated the effect of clomipramine, a tricyclic antidepressant that, when used as a treatment of T. cruzi-chronically infected mice, inhibits trypanothione reductase, an exclusive and vital enzyme of T. cruzi. Clomipramine improved survival (P<0.05) by diminishing the parasite intensity as demonstrated by PCR studies in the heart and skeletal muscle, and significantly prevented the evolution to fibrosis of the inflammatory infiltrates. Clomipramine could be a good candidate for the treatment of chronic Chagas disease.