Research On Effect Of A Purified Laminaria Japonica Polysaccharide On Kidney Injury In Adriamycin-induced Mice

Laminaria japonica is a large marine brown algae,which is abundant in low temperature seawater.The longest is up to about 20 m.Because of prolific and unique taste,it has been widely used for cooking ingredients.Laminar polysaccharide is also known as Kunbu.Previous studies have shown that JP61 A can slow down the aortic vascular calcification and interfere with the process of renal failure.In this paper,the renal injury model induced by adriamycin as a starting point to reseach LJP61 A Laminar polysaccharide in mice with interventional effect in acute renal injury.The intervention mechanism of LJP61 A on foot cell injury was studied in vitro,the results obtained are as follows:(1)Intervention study of LJP61 A on adriamycin-induced renal injury in Balb/c mice: To examine whether the polysaccharides of Laminaria japonica intervened with renal injury,the body weight of mice,pathological sections of kidneys and the biochemical parameters of serum and urine were measured.Histopathological results showed that LJP61 A had some protective effects on glomerular injury and renal fibrosis.Serum biochemical test results showed that LJP61 A can reduce the levels of total cholesterol(TC),triglyceride(TG),urea nitrogen(BUN)and creatinine(Crea),and improve the metabolic disorder of electrolytes and proteins such as Ca2+,Mg2+,and P3+.LJP61 A can significantly delay the development of adriamycin-induced renal injury progression.Further result of staining of HE,Masson,and PAS showed that LJP61 A could significantly protect the stability of glomerular structure,and reduce the damage caused by inflammatory cell infiltration,and slow the glomerular foot process fusion.The toxicity of adriamycin on the foot processes of glomerular epithelial cells protected the glomerular filtration function by LJP61 A.The result of q Real Time-PCR and Western blotting showed that LJP61 A can significantly reduce the expression of inflammatory cytokines IL-1? and TNF-?.LJP61 A inhibit the protein expression of the protein MCP-1,and significantly reduce the expression of the TGF-?1/Smads protein in the signaling pathway of glomerular sclerosis.These results showed that LJP61 A have a significant intervention on adriamycin-induced renal injury.(2)To investigate the interventional effect of LJP61 A on glomerular epithelial cell injury induced by TGF-?1: We build the TGF-?1-induced glomerular epithelial cell transdifferentiation model.Different concentrations of components were set to observe the effect of LJP61 A on glomerular epithelial cell growth.The results showed that LJP61 A promoted cell growth when the concentration was 5-25 ?g/m L.LJP61 A can significantly reduce the damage of glomerular epithelial cell foot processes and maintain cell integrity.The result of q RT-PCR showed that LJP61 A could inhibit the transdifferentiation of glomerular epithelial cells to interphase by the pathway of Smad3/p38 regulating the expression of Nephrin and inhibiting the expression of fibrosis protein ?-SMA Stromal cells.