BACKGROUNDContrast media administration can result in severe nephrotoxicity under pathological conditions such as diabetic nephropathy, congestive heart failure, dehydration, et al. The purpose of this study was to evaluate the effects of dietary hypercholesterolemia on contrast media-induced changes in renal function, blood flow, and histopathology.

METHODSRats were fed either on a normal rodent diet (group N) or a high-cholesterol supplemented diet (group H; 4% cholesterol and 1% cholic acid) for 8 weeks. Half of the animals (n = 6) from each diet group were then given a tail vein injection of 60% diatrizoate (6 ml/kg; group NC and group HC) and the other half were administered saline. Total serum cholesterol, triglyceride, serum creatinine, creatinine clearance rate, fractional excretion of sodium and potassium, and cortical nitric oxide production were determined one day following contrast media administration. Renal blood flow was determined by color Doppler flow imaging and pulsed-mode Doppler. Renal histopathology was observed by light microscopy.

RESULTSTotal serum cholesterol and resistance indices of renal blood vessels increased significantly, while creatinine clearance rate and production of nitric oxide in the renal cortex decreased markedly in group HC and group H when compared to group N and group NC. The creatinine clearance rate decreased significantly in group HC compared to group H. Serum creatinine levels and fractional excretion of sodium and potassium in group HC were significantly higher than those in the other three groups. Severe tubular degeneration and necrosis, protein cast accumulation, and medullary congestion were found in group HC.

CONCLUSIONHypercholesterolemia is a risk factor for contrast media-induced nephropathy. Hypercholesterolemia aggravates contrast media-induced nephrotoxicity through the reduced production of nitric oxide.

Animals ; Cholesterol, Dietary ; toxicity ; Contrast Media ; toxicity ; Kidney Diseases ; chemically induced ; Lipids ; blood ; Male ; Nitric Oxide ; biosynthesis ; Rats ; Rats, Wistar ; Renal Circulation

OBJECTIVE: To explore the effect of niacin on the serum adiponectin concentration in hypercholesterolemia rabbit and the adiponectin concentration secreted by adipocytes in normal rabbits. METHODS: Ten male New Zealand white rabbits fed with high cholesterol diet for 8 weeks were randomly divided into 2 groups: (1) The high cholesterol group maintained a high cholesterol diet for 8 weeks. (2) The same cholesterol diet plus niacin (0.4g/kg*d ) were administrated for 6 weeks in the niacin group. A control group was fed with normal diet for 14 weeks. Subcutaneous adipose from the control group was collected for adipocyte culture. Matured adipocytes were incubated with various concentrations of niacin (0, 0.25, 0.5, 1.0, and 2.0micromol/L). Adiponectin concentrations in the serum and adipocyte culture supernatant were measured by enzyme-linked-immunosorbent assay. RESULTS: Compared with the control group, rabbits in the high cholesterol group showed higher serum levels of total cholesterol, and low density lipoprotein cholesterol (LDL-C), all of which were significantly reduced by niacin treatment (P<0.01),and serum high density lipoprotein-cholesterol (HDL-C) significantly increased (P<0.01). At 8th week, the mean adiponectin concentration of rabbits fed with high cholesterol diet was significantly lower than that of the control group[(1.268+/-0.039)mg/L vs.(1.449+/-0.107)mg/L,P<0.01]. Niacin treatment significantly elevated the serum adiponectin level which was positively related to HDL-C,and negatively related to TC and LDL-C. Cell experiment in vitro indicated that niacin could significantly induce the adiponectin secretion of adipocytes in a dose-dependent manner. CONCLUSION Niacin can significantly promote the adiponectin secretion of adipocytes, suggesting that niacin probably has an ability of elevating the serum adiponectin level in addition to lipid-lowering effect.
Adipocytes ; cytology ; drug effects ; metabolism ; Adiponectin ; blood ; metabolism ; Animals ; Cholesterol ; blood ; Cholesterol, Dietary ; administration & dosage ; toxicity ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; Dose-Response Relationship, Drug ; Hypercholesterolemia ; blood ; etiology ; prevention & control ; Hypolipidemic Agents ; pharmacology ; Male ; Niacin ; pharmacology ; Rabbits ; Random Allocation

OBJECTIVETo investigate the therapeutic effect of emodin on nonalcoholic fatty liver (NAFL) induced by high fat diet in rats.

METHODSNAFL model was established by feeding with high fat diet for 12 weeks in 40 SD rats, confirmed by liver pathologic examination, which were randomly divided into 5 groups: the model control group the mere dietary treatment group (both with distilled water by gastrgarege), the low, moderate and high dose emodin groups treated with emodin 20,40 and 80 mg x kg(-1) x d(-1) once per day respectively. Meanwhile a normal control group was used. The model control group was still fed with high fat diet while the other groups with normal diet. After 4 weeks, body weight, liver index (liver weight/body weight), hepatic function, blood lipid, hepatic lipid and histologic changes were assayed.

RESULTSIn the model control group,body weight, liver index, hepatic enzyme activities, serum lipid and hepatic triglyceride increased significantly (P <0. 05, or P <0. 01), serum high density lipoprotein-cholesterol( HDL-C)decreased (P <0.01 ), and moderate to severe hepatocyte steatosis was observed, while these indexes were all improved significantly in the 3 emodin groups; hepatic histologic changes were improved in the mere dietary treatment group, however, high level of ALT and hyperlipidemia persisted.

CONCLUSIONEmodin combined with dietary therapy is effective for NAFL rats induced by high fat diet.

Animals ; Cholesterol, HDL ; blood ; Dietary Fats ; toxicity ; Drugs, Chinese Herbal ; therapeutic use ; Emodin ; therapeutic use ; Fatty Liver ; diet therapy ; drug therapy ; etiology ; Rats ; Rats, Sprague-Dawley

To investigate the temporal progression of atherogenesis on the aorta and involvement of the monocyte-macrophage system in the liver and spleen, we fed 74 rabbits with high fat (14 or 7 gm+ACU-) and cholesterol (2 and 1+ACU-) diets for 4 to over 24 weeks. Using both light and electron microscopies, we found that the bro-fatty areas on the luminal surface of aortas was spread over along the eding time dependently. The fat deposits also in the liver and spleen worsened pending on the time of feeding the atherogenic diets. Not only nocyte-derived foam cells, but also parenchymatous cells in the liver and leen involved become fat-laden cells. According to these results, we propose at there are three stages: 1) the primary seeding, 2) the intermediate turing and 3) the advanced periods. These periods may play very important les in designing the management and treatment of atherosclerotic patients.
Animal ; Aorta/pathology ; Aorta/drug effects+ACo- ; Aortic Diseases/pathology+ACo- ; Aortic Diseases/etiology ; Arteriosclerosis/pathology+ACo- ; Arteriosclerosis/etiology ; Cholesterol, Dietary/toxicity ; Diet, Atherogenic+ACo- ; Dietary Fats/toxicity+ACo- ; Dose-Response Relationship, Drug ; Fatty Liver/pathology+ACo- ; Fatty Liver/etiology ; Female ; Liver/pathology ; Liver/drug effects+ACo- ; Male ; Microscopy, Electron ; Rabbits ; Spleen/pathology ; Spleen/drug effects+ACo- ; Splenic Diseases/pathology+ACo- ; Splenic Diseases/etiology ; Time Factors

To investigate the temporal progression of atherogenesis on the aorta and involvement of the monocyte-macrophage system in the liver and spleen, we fed 74 rabbits with high fat (14 or 7 gm+ACU-) and cholesterol (2 and 1+ACU-) diets for 4 to over 24 weeks. Using both light and electron microscopies, we found that the bro-fatty areas on the luminal surface of aortas was spread over along the eding time dependently. The fat deposits also in the liver and spleen worsened pending on the time of feeding the atherogenic diets. Not only nocyte-derived foam cells, but also parenchymatous cells in the liver and leen involved become fat-laden cells. According to these results, we propose at there are three stages: 1) the primary seeding, 2) the intermediate turing and 3) the advanced periods. These periods may play very important les in designing the management and treatment of atherosclerotic patients.
Animal ; Aorta/pathology ; Aorta/drug effects+ACo- ; Aortic Diseases/pathology+ACo- ; Aortic Diseases/etiology ; Arteriosclerosis/pathology+ACo- ; Arteriosclerosis/etiology ; Cholesterol, Dietary/toxicity ; Diet, Atherogenic+ACo- ; Dietary Fats/toxicity+ACo- ; Dose-Response Relationship, Drug ; Fatty Liver/pathology+ACo- ; Fatty Liver/etiology ; Female ; Liver/pathology ; Liver/drug effects+ACo- ; Male ; Microscopy, Electron ; Rabbits ; Spleen/pathology ; Spleen/drug effects+ACo- ; Splenic Diseases/pathology+ACo- ; Splenic Diseases/etiology ; Time Factors