Abstract
Oxidative stress has crucial role in pathogenesis of diabetic nephropathy (DN). Despite satisfactory results from antioxidant therapy in rodent, antioxidant therapy showed conflicting results in combat with DN in diabetic patients. Directory of Open Access Journals (DOAJ), Google Scholar,Pubmed (NLM), LISTA (EBSCO) and Web of Science have been searched. Treatment of DN in human are insufficient with rennin angiotensin system (RAS) blockers, so additional agent ought to combine with this management. Meanwhile based on DN pathogenesis and evidences in experimental and human researches, the antioxidants are the best candidate. New multi-property antioxidants may be improved human DN that show high power antioxidant capacity, long half-life time, high permeability to mitochondrion, improve body antioxidants enzymes activity and anti-inflammatory effects. Based on this review and our studies on diabetic rats, rosmarinic acid a multi-property antioxidant may be useful in DN patients, but of course, needs to be proven in clinical trials studies.
Highlights
Based on this review and our studies on diabetic rats, rosmarinic acid a multi-property antioxidant may be useful in diabetic nephropathy (DN) patients, but needs to be proven in clinical trials studies
Implication for health policy/practice/research/medical education: Treatment of diabetic nephropathy (DN) in human by rennin angiotensin system blockers is inadequate and antioxidants ought to couple with this treatment
Rosmarinic acid, multi properties antioxidant may be useful in DN patients, but needs to be proven in clinical trials studies
Summary
Several mechanisms are thought to be involved in the pathogenesis of diabetic nephropathy and its complications, all of them originating from hyperglycemia Some of these pathways are: increasing and activation of intra-renal rennin angiotensin system (RAS), formation of advanced glycation end products (AGEs), polyol pathway activation, aldol reductase activation, activation of protein kinase C (PKC), increase of some cytokines – such as insulin like growth factor-1 (IGF1), transforming growth factor beta (TGF-β)- and the oxidative stress pathway [1,2,3,4,5]. There are many evidences that oxidative stress plays a key role in the most pathogenic pathways of diabetic complications [6] Free radicals such as superoxide can induce cell and tissue injuries throughout lipid peroxidation, activation of nuclear factor of Kappa-Beta [7], production of peroxynitrite, PKC activation and induction of apoptosis. Inhibition of oxidative stress may constitute a focal point for multiple therapeutic synergies
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