Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0020473 (
hyperlipidemia
)
15,891
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The present work includes a study on the glycosaminoglycanuric condition induced by adriamycin (
ADR
, a chemotherapeutic agent) and the accompanying secondary
hyperlipidemia
, wherein the treatment with a low-molecular-weight heparin-derivative (LMWH), certoparin, is evaluated for its protective role (if any) on these parameters. Two groups of male albino rats of the Wistar strain (140+/-10 g) received a single intravenous injection of adriamycin (7.5 mg/kg), and one of these groups was treated with a low-molecular-weight heparin-derivative (Certoparin Sodium, Troparin; 300 microg/day/rat s.c.), commencing on day 8, for a week. Urinary total glycosaminoglycans excretion of the untreated
ADR
-induced group was found to increase on the 8th and the 15th days of observation, when compared with the controls. The LMWH treatment commencing on day 8 resulted in minimising the glycosaminoglycans (GAGs) excretion by day 15 (p<0.001). Plasma, cardiac, hepatic and renal lipids (cholesterol, triglycerides and phospholipids) showed a sharp increase in the pathologic group, along with a rise in plasma LDL and VLDL cholesterol and drop in HDL cholesterol levels, paralleled by abnormal activities of the enzymes involved in lipid metabolism. LMWH treated group showed a normalised lipid profile and the activities of the lipid-metabolising enzymes was close to that of controls. It is concluded herein that adriamycin administration resulted in severe nephropathy manifested by increased glycosaminoglycanuria and abnormal lipid metabolism, and that LMWH treatment afforded substantial protection by restoring glomerular structure and function, and normalised the plasma and tissue lipid levels, lipoprotein profile and the activities of lipid-metabolising enzymes.
...
PMID:Beneficial cardio-renovascular effects of a low-molecular-weight heparin-derivative on adriamycin-induced glycosaminoglycanuria and tissue lipid abnormalities. 1586 50
Adriamycin is a potent anticancer agent, its clinical use is limited for its marked cardiotoxicity and nephrotoxicity. The present study aimed to investigate the possible protective role of the natural antioxidant silymarin on
ADR
-induced heart and kidney toxicity. Studies were performed on four groups of rats. 1--control group, 2--silymarin group (50 mg/kg), 3--adriamycin group (10 mg/kg), 4--adriamycin+silymarin group. On the third day after
ADR
injection, plasma was separated for determination of LDH, CPK, cholesterol and total lipids. 30 days after
ADR
injection, plasma was separated for determination of creatinine and urea levels. Frozen heart specimens (72 h) and frozen kidney specimens (30days) were used for estimation of lipid peroxides and GSH contents. Histopathological examinations of heart and kidney sections were also done. Pretreatment of
ADR
-treated rats with silymarin resulted in a significant decrease in the plasma CPK, LDH, creatinine and urea. On the other hand silymarin pretreatment did not change
ADR
-induced
hyperlipidemia
. Silymarin pretreatment significantly decreased the myocardial MDA contents. In addition, silymarin pretreatment normalized renal tissue contents of MDA and GSH. Histopathological examination of heart and kidney sections revealed that
ADR
caused only mild myocardial injury in silymarin pretreated rats. Also, silymarin pretreatment inhibited
ADR
-induced renal tubular damage in rats. These results have suggested that, silymarin ameliorated
ADR
-induced cardiotoxicity and protected against
ADR
-induced nephrotoxicity in male albino rats. The mechanisms of silymarin induced protection against
ADR
-induced toxicities were proved to be due to inhibition of lipid peroxidation and protection against GSH depletion.
...
PMID:Silymarin prevents adriamycin-induced cardiotoxicity and nephrotoxicity in rats. 1848 2