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[Background / Purpose This paper is divided into three parts. First, we nephritis rehabilitation tablets in the treatment of chronic kidney disease (Chronic kidney disease, CKD) Research Profile. The nephritis Rehabilitation piece traditional Chinese medicine, spleen and kidney, Thanh Hoa heat, blood circulation and other effects. Domestic nephritis rehabilitation piece clinical pharmacodynamic study in the field of kidney disease, chronic glomerulonephritis, nephrotic syndrome, IgA nephropathy, diabetic nephropathy, chronic renal insufficiency common primary and secondary sexual CKD. Its clinical efficacy in improving the corresponding clinical signs of disease, reduce proteinuria, hematuria, and can also improve renal function. Nephritis rehabilitation tablets in the treatment of CKD pharmacological effects, including suppression of the immune response, reduce inflammation and damage, renal fibrosis, the protection of podocytes and tubular epithelial cells. Second, we summarize the intervention of CKD kidney tissue inflammation signaling pathway the p38MAPK adjustment mechanism and Chinese medicine. Kidney tissue inflammation and its associated tissue injury (such as glomerulosclerosis and renal interstitial fibrosis) is an important factor in the progression of CKD to ESRD. p38MAPK signaling pathway to regulate expression and biological activity of a variety of nuclear transcription factor, can also affect the synthesis of a variety of downstream inflammatory mediators, and to participate in the activation of inflammatory cells, play an important role in the inflammatory injury of the kidney disease. Studies have shown that some single herb and its extracts as well as some Chinese herbal compound can affect the renal tissue inflammatory response by regulating p38 MAPK signal pathway and, thus, reduce the inflammation of the kidney tissue injury. Finally, as the focus of this article, we reported nephritis rehabilitation sheet adjustment in renal tissue p38 MAPK signal pathway and improve with adriamycin (Adriamycin-induced nephropathy, ADRN) model of renal molecular mechanisms of tissue inflammation injury. We use the method of unilateral nephrectomy and intravenous injection of doxorubicin (Adriamycin, ADR), establish ADRN model, the observed nephritis rehabilitation sheet on the renal tissue inflammation signaling pathway p38MAPK intervention role, trying to clarify the nephritis rehabilitation piece in the body by regulating the p38MAPK signaling pathways, molecular mechanisms that reduce glomerular transforming growth factor (Transforming growth factor, TGF)-beta1 expression and macrophage cells (macrophage, macrophages were) infiltration, improve renal tissue inflammatory injury. [Methods] 19 SD rats methods were randomly divided into sham operation group, control group and nephritis rehabilitation tablet group. The nephritis rehabilitation tablet group and the control group rats underwent right kidney removal surgery, and in 4 weeks by intravenous injection of doxorubicin (4 or 2 mg kg-1), establish ADRN model. After the second injection, ADR, the nephritis rehabilitation piece group rats by oral gavage nephritis rehabilitation piece 1.2g · kg-1 · d-1, and intervene in the control group with distilled water at the same time, a total of four weeks intervention. Week after weighing the body weight of rats and detects 24h urinary protein excretion. Weekend after the rats were killed, draw blood, removal of the left kidney and weighed observed glomerular macrophage cells ED1 and ED3 infiltration, podocytes and filtration membrane ultrastructure, alpha-smooth muscle actin (alpha -smoothmuscle actin, alpha-SMA), the expression of type I collagen (Collagen type I) and glomerular morphological characteristics, serum biochemical indicators, and by means of Western blotting analysis in renal tissue TGF-beta1 phosphorylation p38MAPKC the Phosphoryl ated of p38MAPK, p -p38MAPK) protein expression. [Results] The the nephritis rehabilitation piece reduced glomerular macrophage cells ED1 the ED3 infiltration, down a rat model of renal tissue TGF-beta 1 and p-p38 MAPK protein expression, inhibition of the model rat mesangial cells (mesangial cell, MC) proliferation, deposition of extracellular matrix (Extracellular matrix, ECM) and collagen (Collagen type I), to reduce the alpha-SMA, type I collagen expression, it is also improved mouse model of proteinuria and serum albumin (Albumin, Alb) However, serum urea nitrogen (Blood urea nitrogen, BUN) and serum creatinine (serum creatinine, Scr). [Conclusion] nephritis rehabilitation piece has a role to reduce the inflammation of the renal tissue damage in the body; nephritis rehabilitation piece by lowered renal tissue p38 MAPK signal pathway in key signaling molecules - p-p38MAPK protein expression intervention p38 MAPK signal pathway signal transduction, reducing glomerular TGF-beta1 expression and macrophage infiltration, thereby improving renal tissue inflammation injury.
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