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Decreased Inflammation (decreased + inflammation)
Selected AbstractsSilibinin attenuates cardiac hypertrophy and fibrosis through blocking EGFR-dependent signaling,JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 5 2010Wen Ai Abstract Cardiac hypertrophy is a major determinant of heart failure. The epidermal growth factor receptor (EGFR) plays an important role in cardiac hypertrophy. Since silibinin suppresses EGFR in vitro and in vivo, we hypothesized that silibinin would attenuate cardiac hypertrophy through disrupting EGFR signaling. In this study, we examined this hypothesis using neonatal cardiac myocytes and fibroblasts induced by angiotensin II (Ang II) and animal model by aortic banding (AB) mice. Our data revealed that silibinin obviously blocked cardiac hypertrophic responses induced by pressure overload. Meanwhile, silibinin markedly reduced the increased generation of EGFR. Moreover, these beneficial effects were associated with attenuation of the EGFR-dependent ERK1/2, PI3K/Akt signaling cascade. We further demonstrated silibinin decreased inflammation and fibrosis by blocking the activation of NF-,B and TGF-,1/Smad signaling pathways in vitro and in vivo. Our results indicate that silibinin has the potential to protect against cardiac hypertrophy, inflammation, and fibrosis through blocking EGFR activity and EGFR-dependent different intracellular signaling pathways. J. Cell. Biochem. 110: 1111,1122, 2010. Published 2010 Wiley-Liss, Inc. [source] Estrogen attenuated markers of inflammation and decreased lesion volume in acute spinal cord injury in ratsJOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2005Eric Anthony Sribnick Abstract Spinal cord injury (SCI) is a devastating neurologic injury with functional deficits for which the only currently recommended pharmacotherapy is high-dose methylprednisolone, which has limited efficacy. Estrogen is a multiactive steroid that has shown antiinflammatory and antioxidant effects, and estrogen may modulate intracellular Ca2+ and attenuate apoptosis. For this study, male rats were divided into three groups. Sham group animals received a laminectomy at T12. Injured rats received both laminectomy and 40 g · cm force SCI. Estrogen-group rats received 4 mg/kg 17,-estradiol (estrogen) at 15 min and 24 hr post-injury, and vehicle-group rats received equal volumes of dimethyl sulfoxide (vehicle). Animals were sacrificed at 48 hr post-injury, and 1-cm-long segments of the lesion, rostral penumbra, and caudal penumbra were excised. Inflammation was assessed by examining tissue edema, infiltration of macrophages/microglia, and levels of cytosolic and nuclear NF,B and inhibitor of kappa B (I,B,). Myelin integrity was examined using Luxol fast blue staining. When compared to sham, vehicle-treated animals revealed increased tissue edema, increased infiltration of inflammatory cells, decreased cytosolic levels of NF,B and I,B,, increased levels of nuclear NF,B, and increased myelin loss. Treatment of SCI rats with estrogen reduced edema and decreased inflammation and myelin loss in the lesion and penumbral areas, suggesting its potential as a therapeutic agent. Further work needs to be done, however, to elucidate the neuroprotective mechanism of estrogen. © 2005 Wiley-Liss, Inc. [source] The Emerging Role of Flavonoid-Rich Cocoa and Chocolate in Cardiovascular Health and DiseaseNUTRITION REVIEWS, Issue 3 2006Mary B. Engler PhD Cocoa and chocolate have recently been found to be rich plant-derived sources of antioxidant flavonoids with beneficial cardiovascular properties. These favorable physiological effects include: antioxidant activity, vasodilation and blood pressure reduction, inhibition of platelet activity, and decreased inflammation. Increasing evidence from experimental and clinical studies using cocoa-derived products and chocolate suggest an important role for these high-flavanol-containing foods in heart and vascular protection. [source] Nontuberculous Mycobacteria-Induced Parotid Lymphadenitis Successfully Limited With Clarithromycin and RifabutinTHE LARYNGOSCOPE, Issue 8 2004Maulik B. Shah Abstract Objectives/Hypothesis: Nontuberculous mycobacterial adenitis of the parotid gland is often difficult to diagnose. The rarity of these infections in the parotid region and the lack of specific guidelines pose a treatment challenge to the clinician. Three cases of nontuberculous mycobacterial adenitis are presented, with clinical response to antibiotics before surgery. Study Design: Retrospective chart review was made of children up to 18 years of age presenting with a parotid mass diagnosed as nontuberculous mycobacterial infection. Methods: Three patients (age range, 15 to 30 mo) with nontuberculous mycobacteria-induced parotid lymphadenitis were treated with a combination antibiotic regimen of clarithromycin and rifabutin or with clarithromycin alone. Results: All three patients responded clinically to the antibiotic treatment as evidenced by a smaller mass size and resolution of the overlying discoloration. Subsequent parotidectomy or biopsy appeared to be easier to perform because of decreased inflammation and edema and a more readily dissectible facial nerve. Conclusion: Children with nontuberculous mycobacteria-induced parotid lymphadenitis should be started on a trial of antibiotic treatment before surgery. Although surgery remains the definitive treatment modality, a larger study of preoperative antibiotic use against nontuberculous mycobacterial adenitis of the parotid in children is necessary. [source] Pathology is alleviated by doxycycline in a laminin-,2,null model of congenital muscular dystrophyANNALS OF NEUROLOGY, Issue 1 2009Mahasweta Girgenrath PhD Objective Congenital muscular dystrophy type 1A is an autosomal recessive disease that is caused by loss-of-function mutations in the laminin-,2 gene, and results in motor nerve and skeletal muscle dysfunction. In a previous study, we used genetic modifications to show that inappropriate induction of apoptosis was a significant contributor to pathogenesis in a laminin-,2,deficient mouse model of congenital muscular dystrophy type 1A. To identify a possible pharmacological therapy for laminin-,2 deficiency, we designed this study to determine whether treatment with minocycline or doxycycline, which are tetracycline derivatives reported to have antiapoptotic effects in mammals, would significantly increase lifespan and improve neuromuscular function in laminin-,2,deficient mice. Methods Mice that were homozygous for a targeted, inactivating mutation of the laminin-,2 gene were placed into control, minocycline-treated, or doxycycline-treated groups. Drug treatment began within 2 weeks of birth, and the progression of disease was followed over time using behavioral, growth, histological, and molecular assays. Results We found that treatment with either minocycline or doxycycline increased the median lifespan of laminin-,2,null mice from approximately 32 days to approximately 70 days. Furthermore, doxycycline improved postnatal growth rate and delayed the onset of hind-limb paralysis. Doxycycline-treated laminin-,2,deficient muscles had increased Akt phosphorylation, decreased inflammation, and decreased levels of Bax protein, terminal deoxynucleotidyltransferase,mediated dUTP nick end labeling,positive myonuclei, and activated caspase-3. Interpretation Doxycycline or other drugs with similar functional profiles may be a possible route to improving neuromuscular dysfunction caused by laminin-,2-deficiency. Ann Neurol 2008 [source] Anti-Inflammatory Activity of a New Class of Nitric Oxide Synthase Inhibitors That Release Nitric OxideCHEMMEDCHEM, Issue 10 2008Maurizio Botta Prof. Abstract Nitric oxide (NO) is a gaseous mediator that exerts key regulatory functions in mammalian cells. Low levels of NO exert homeostatic functions and counteract inflammation, whereas high amounts of NO cause tissue destruction and cellular death. Herein we describe a new class of nitric oxide synthase (NOS) inhibitor NO-donating drugs (NI-NODs). Human endothelial cells and human monocyte-based activity screening showed that NI-NODs inhibit IL-1, production, modulate PGE2 production, and protect against apoptosis. In a rodent model of colitis, NI-NOD1 and NI-NOD2 potently decreased inflammation. These data show that NI-NODs are effective in both in,vitro and in,vivo models of inflammation, mimicking the positive effects of low levels of NO and suppressing NOS-induced NO production. [source] | |||||||||||||