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Inflammation Mechanism of Myocardial Fibrosis in Rats

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Inflammation Mechanism of Myocardial Fibrosis in Rats  Empty Inflammation Mechanism of Myocardial Fibrosis in Rats

Post  knowing Sat Jul 16, 2011 5:50 am

Chronic, subclinical of inflammation, and inflammation leads to insulin resistance in type 2 diabetes and atherosclerosis of the common pathological basis. One is characterized by inflammatory factors and inflammatory markers. Such as CRP, TNF-a, IL-6 and adiponectin, resistin and leptin. The second characteristic is the activation of inflammatory signaling pathways. Inhibitor of nuclear factor κB kinase (IκB-kinase, IKK) nuclear factor κB (NF-κB) inhibitor (IκB) kinase, and NF-κB is the inflammation starts, adjust the key factor. NF-κB and IκB inhibitor combined to form inactive cytoplasm, IKK by TNF-α, IL-1, IL-6 and other inflammatory factors in activated, the phosphorylation of IκB and NF-κB dissociation, disinhibition of the activity of NF-κB into the cell, regulating a range of inflammatory cytokines and inflammation-related substances in gene transcription and protein synthesis. Diabetic cardiomyopathy is an independent cardiovascular complications of diabetes, and diabetes patients's heart failure incidence and high mortality rates are closely related. Remodeling and myocardial interstitial fibrosis is characteristic of diabetic cardiomyopathy pathology, diabetes, myocardial fibrosis has been clearly involved in the regulation of factors renin - angiotensin - aldosterone system (RAAS), endothelin, NO, sugar-based of end products (AGEs), matrix metalloproteinases, TGF-β1 and so on.while rosiglitazone hydrochloride and atorvastatin,and their combination can protect it .


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Join date : 2011-04-20

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