| Background:Diabetes mellitus (DM) is an ever-growing problem world wide. Diabetic nephropathy(DN) is the main cause of increased mortality and morbidity in DM patients. Approximately 40% of the patients with diabetes will develop diabetic kidney disease. In the United States, diabetes has become the most common single cause of endstage renal disease defined by the need for dialysis or transplantation. Prevention or delay of DN development has become the hot point of diabetic research.Diabetic nephropathy is characterized by the hypertrophy of both glmerular and tubuloepitheliar elements, thickness of the basement membrane, and accumulation of extracellular matrix (ECM) in the glomerular mesangium and the interstitium. The pathogenesis of DN is a synthetic result initiated by hyperglycemia or disorders of lipid metabolism and many factors including vascular active substances, growth factors, cellular intermediator and chemotactic factors are involved in.In the streptozotocin-induced diabetic rats model, diabetic renal hypertrophy has been well characterized: the robust hypertrophic response is the predominant finding accounting for increased kidney weight, although a delayed minor component of cellular hyperplasia is also seen. Several lines of evidence point to a causal link between upregulation of the renal transforming growth factorP(TGF-P) system and the development of renal hypertrophy in diabetes. A number of mechanism have been implicated in the upregluation of TGF-P in diabetes. Glucose can induce production of a variety of factors in vitro, including angiotensin Ⅱ (Ang Ⅱ), thromboxane, endothelin, and platelet-drived growth factor. All of these have been shown to induce TGF-p production.The kidney both produces TGF-p and is a target of TGF-p action as TGF-PmRNA. Evidence in these studies further suggests that TGF-β1 is a key factor in the induction ofdiabetic renal hypertrophy. In vitro, TGF-β1 has been shown to modulate extracellular matrix production. Of relevance, both glomerular mesangial and epithelial cells increase synthesis of extracellular matrix proteins in response to TGF-β1. In addition, TGF-β1 inhibits the synthesis of collagenases and stimulates tissue production of metalloproteinase inhibitors.Together, these mechanisms could lead to the extracellular matrix, thereby contributing to matrix accumullation.It is now thought that the vascular active matter such as Ang II plays a pivotal role in meadiating various forms of renal injury, including DN. Ang II has multiple actions.It not only is a potent vasoconstrictor, but also has strong trophic properties. It can accelerate the progress of renal interstitial fibrosis. Consenquently, blocking Ang II should attenuate the progession of DN. In early experimental studies, angiotensin converting enzyme inhibitor (ACEI) dosedependently decreased TGF-β1 mRNA expression and cellular hypertrophy. This activity was additional to the effects on intrarenal haemodynamics.The symtoms of diabetic and kidney disease are similar to those of 'subdue thirsty disease','hydroncus', 'urine turbid', 'consumptive disease' in traditional Chinese medicine. The Chinese medical pathogenesis of DN is mainly Deficiency of Qi and Yin early, and Dificiency of Yin and Yang late. Blood stasis and turbid dampness exist all through. The pathogenesis of DN is deficiency syndromes and redundancy sydromes mixed and reciprocal caused,so eliminate evils for supporting vital Qi,reinforce and reduce concurrently are the main treatment principles.Gui Qi Mixture (GQM) was consisted of Astragalus Membranace and Angelica sinensis.These two natual druge possese extensive pharmacol action. They can regulate serum lipid, relieve lipid peroxidation, inhibit platelet aggregation, reduce serum creatinine, proteinuria, glomerulosclerosis and the expression of TGF-β1.In the present study, the clinical effects of Chinese Medical therapy of YiQiHuoXue method (invigorating Qi-activating the blood) and GQM were investigated and compared with ACEI in streptozotocin-induced diabetic rats mainly with...
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