Objective To investigate the influence of sodium selenite on the expression of adiponectin and nephrin in the kidney of rats with diabetic nephropathy, the relation of sodium selenite with adiponectin and nephrin, and to study the roles played by these factors in diabetic nephropathy. Methods Rat models of diabetic nephropathy were established by injecting intraperitoneally streptozocin combined with high fat diet. Three groups of rats were employed: control group, diabetic nephropathy group, and selenite-treated group. The selenite-treated rats were given selenite solution by intragastric administration every day, and other groups were given same volume of saline. After 10 weeks, all rats were sacrificed, blood and urine samples were collected. The kidneys were used to observe pathological changes with light microscope, and to locate protein expression with immunohistochemistry analysis. The mRNA and protein expressions of adiponectin and nephrin were analyzed via real-time PCR, RT PCR, and Western blot. Results The basic condition, biochemical parameters, and pathological images in selenite-treated group were better than those in diabetic nephropathy group. Immunohistochemistry analysis showed that the expression of adiponectin was in both glomeruli and renal tubules in selenite-treated group, and the coloration was enhanced as compared with diabetic nephropathy group. The mRNA and protein expressions of adiponectin in selenite-treated group were significantly higher than those in diabetic nephropathy group and the control group (all P＜0. 05 ). Nephrin expression in selenite-treated group was also higher than that in diabetic nephropathy group, but lower than that in control group. Conclusion Sodium selenite can enhance the mRNA and protein expressions of adiponectin and nephrin in kindey of rats with diabetic nephropathy. Sodium selenite,adiponectin, and nephrin may play important roles in delaying and preventing the development of diabetic nephropathy.

Ulcerative colitis(UC)is characterized by chronic relapsing intestinal inflammation.Currently,there is no effective treatment for the disease.According to our preliminary data,1,8-cineole,which is the main active compound of Amomum compactum Sol.ex Maton volatile oil and an effective drug for the treat-ment of pneumonia,showed remarkable anti-inflammatory effects on colitis pathogenesis.However,its mechanism of action and direct targets remain unclear.This study investigated the direct targets and mechanism through which 1,8-cineole exerts its anti-inflammatory effects using a dextran sulfate so-dium salt-induced colitis mouse model.The effects of 1,8-cineole on macrophage polarization were investigated using activated bone marrow-derived macrophages and RAW264.7 cells.In addition,1,8-cineole targets were revealed by drug affinity responsive target stability,thermal shift assay,cellular thermal shift assay,and heat shock protein 90(HSP90)adenosine triphosphatases(ATPase)activity assays.The results showed that 1,8-cineole exhibited powerful anti-inflammatory properties in vitro and in vivo by inhibiting the macrophage M1 polarization and protecting intestinal barrier function.Mech-anistically,1,8-cineole directly interacted with HSP90 and decreased its ATPase activity,also inhibited nucleotide-binding and oligomerization domain-,leucine rich repeat-,and pyrin domain-containing 3(NLRP3)binding to HSP90 and suppressor of G-two allele of SKP1(SGT1)and suppressed NLRP3 inflammasome activation in macrophages.These results demonstrated that 1,8-cineole is a potential drug candidate for UC treatment.