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Oxidative Stress: Harms and Benefits for Human Health
- G. Pizzino, N. Irrera, +6 authors A. Bitto
- Biology, Medicine
- Oxidative medicine and cellular longevity
- 27 July 2017
In this review, the most recent findings in the oxidative stress field are described, highlighting both its bad and good sides for human health. Expand
Effects of Genistein and Hormone‐Replacement Therapy on Bone Loss in Early Postmenopausal Women: A Randomized Double‐Blind Placebo‐Controlled Study
- N. Morabito, A. Crisafulli, +10 authors F. Squadrito
- Journal of bone and mineral research : the…
- 1 October 2002
Genistein‐positive effects on bone loss already observed in the experimental models of osteoporosis are confirmed and indicates that the phytoestrogen reduces bone resorption and increases bone formation in postmenopausal women. Expand
Effects of the Phytoestrogen Genistein on Bone Metabolism in Osteopenic Postmenopausal Women
In postmenopausal women, treatment with genistein increased bone mineral density at the lumbar spine and femoral neck with no clinically significant adverse effects on the breast and uterus, and the mechanism of action of Genistein on bone is not yet fully understood. Expand
Nuclear factor kappa-B blockade reduces skeletal muscle degeneration and enhances muscle function in Mdx mice
The hypothesis that NF-kappaB contributes to the perpetuation of the dystrophic damage and its blockade produces beneficial effects on functional, biochemical, and morphological parameters in mdx mice is supported and may have clinical implications for the pharmacological treatment of patients with DMD. Expand
The effect of the phytoestrogen genistein on plasma nitric oxide concentrations, endothelin-1 levels and endothelium dependent vasodilation in postmenopausal women.
Genistein therapy improves flow-mediated endothelium dependent vasodilation in healthy postmenopausal women and may be mediated by a direct effect of genistein on the vascular function and could be the result of an increased ratio of nitric oxide to endothelin. Expand
Lipid peroxidation inhibition blunts nuclear factor-kappaB activation, reduces skeletal muscle degeneration, and enhances muscle function in mdx mice.
- S. Messina, D. Altavilla, +8 authors G. Vita
- Biology, Medicine
- The American journal of pathology
- 1 March 2006
The data suggest that oxidative stress/lipid peroxidation represents one of the mechanisms activating NF-kappaB and the consequent pathogenetic cascade in mdx muscles, and may have clinical implications for the pharmacological treatment of patients with DMD. Expand
Antiobesity and cardiovascular toxic effects of Citrus aurantium extracts in the rat: a preliminary report
The data indicate that, in the rat, antiobesity effects of C. aurantium are accompanied by toxic effects probably due to cardiovascular toxicity. Expand
Both early and delayed treatment with melanocortin 4 receptor-stimulating melanocortins produces neuroprotection in cerebral ischemia.
Treatment with nanomolar doses of the melanocortin analog [Nle4, D-Phe7] alpha-MSH modulated the inflammatory and apoptotic cascades and reduced hippocampus injuries even when delayed up to 9 h after ischemia, with consequent dose-dependent improvement in subsequent functional recovery. Expand
Flavocoxid, a dual inhibitor of cyclooxygenase and 5‐lipoxygenase, blunts pro‐inflammatory phenotype activation in endotoxin‐stimulated macrophages
- D. Altavilla, F. Squadrito, +4 authors L. Minutoli
- Biology, Medicine
- British journal of pharmacology
- 1 August 2009
The anti‐inflammatory activity of flavocoxid in rat peritoneal macrophages stimulated with Salmonella enteritidis lipopolysaccharide (LPS) was investigated. Expand
Inhibition of lipid peroxidation restores impaired vascular endothelial growth factor expression and stimulates wound healing and angiogenesis in the genetically diabetic mouse.
Evidence is provided that lipid peroxidation inhibition restores wound healing to nearly normal levels in experimental diabetes-impaired wounds and normalizes the defect in VEGF regulation associated with diabetes-induced skin-repair disorders. Expand