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Kandungan Kimia Meniran mengandung golongan senyawa kimia golongan flavonoid, antara lain quercetin, quercetrin, isoquercetrin, astragalin,

rutin kaemperol-4-rhamnopyranoside, eriodictyol-7-rhamnopyranoside, fisetin-4-O-glicoside, 5,6,7,4-tetrahydroxy-8-(3methylbut-2-enyl)-flavonone-5-O-runoside (nirurin). Pada akarnya terdapat 3,5,7trihydroxyflavonl-4-O-_-L-(-) rhamnopyranoside; suatu senyawa glikosida flavonoid dengan kaemperol sebagai aglikon dan rhamnosa sebagai bagian glikon. Ikatan glikosida terdapat pada posisi 4 sebagai gliksida flavonoid terdapat pula 5,3,4;rihydroxyflavononone-7-O-_-L-(-), suatu flavonone (eriodictyol); L(-)-rhamnose sebagai bagian gikon. Disamping itu terdapat senyawa lignan, norsecurinine, securinine, allosecurinine, dan senyawa alkaloid (entnorsecurinine). Ignan; nirphyllin (3,3,5,9,9-pentamethoxy-4-hydroxy,4,5-methylendioxylignan, phyllnirurin (3,4methylendioxy-5-methoxy-9-hidroxy-4-7-epoxy-8,3-neolignan),isolintetrain, hypophyllanthin (tidak pahit). Nirtetralin,niranthin, phyllanthin (pahit), hinikinin, ligtetralin, phyllanthostatin A, dan alkaloid dari trans-phytol (Sudarsono dkk., 1996).

Effects of quercetin on apoptosis, NF-B and NOS gene expression in renal ischemia/reperfusion injury Authors: M. Kenan Kinaci, Nilufer Erkasap, Aysegul Kucuk, Tulay Koken, Murat Tosun Affiliations: Department of Physiology, Eskisehir Osmangazi University Medical Faculty, Eskisehir 26480, Turkey, Department of Physiology, Kutahya Dumlupinar University Medical Faculty, Kutahya, Turkey, Department of Biochemistry, Afyon Kocatepe University Medical Faculty, Afyon, Turkey, Department of Histology and Embryology, Afyon Kocatepe University Medical Faculty, Afyon, Turkey Published online on: Wednesday, November 16, 2011 Doi: 10.3892/etm.2011.382 Pages: 249-254 Abstract: The aim of this study was to investigate the effects of quercetin on nitric oxide synthase (NOS), nuclear factor-B (NF-B) and apoptosis in renal ischemia/reperfusion (I/R) injury in rats. A total of 42 Sprague-Dawley rats were divided into three groups. The control, I/R and I/R+quercetin (I/R+Q) groups were treated with quercetin (50 mg/kg intraperitoneal) 1 h prior to the induction of ischemia. Tissue malondialdehyde (MDA) and glutathione (GSH) levels were determined by high-performance liquid chromatography (HPLC). p53, endothelial NOS (eNOS) and NF-B expression were assessed immunohistochemically, and apoptosis assesment was performed using terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) assay. The mRNA levels of inducible NOS (iNOS) in renal tissue were determined by real-time polymerase chain reaction (RT-PCR). MDA levels were significantly decreased in the quercetin group compared to the I/R group. However,

GSH levels were significantly increased with quercetin treatment in the I/R group. Histological results, the number of apoptotic and p53-positive cells, NF-B and eNOS expression levels were significantly decreased in the quercetin treatment group compared to the I/R group. iNOS gene expression increased in the I/R group, but no significant difference was found between the I/R and quercetin treatment groups. Therefore, quercetin not only has antioxidant and anti-apoptotic activities, but also has an inhibitory effect on eNOS and NFB for renal tissue protection during I/R injury in rats. Therefore, quercetin may be a promising renoprotective therapeutic agent.

Protective effect of quercetin on renal ischemia/reperfusion injury in rats. (PMID:12768068)


Abstract Citations BioEntities Related Articles

Kahraman A, Erkasap N, Serteser M, Kken T Department of Biochemistry, The School of Medicine, Kocatepe University, Afyon-03200, Turkey. ahmetkah@aku.edu.tr Journal of Nephrology [2003, 16(2):219-24] Type: Journal Article, Comparative Study Abstract
BACKGROUND: There is increasing evidence to suggest that toxic oxygen radicals play a role in the pathogenesis of ischemia/reperfusion (I/R) injury in the kidney. The aim of this study was to evaluate whether quercetin, an oxygen free radical scavenger, protects kidney tissue. METHODS: A renal I/R injury was induced by a left renal pedicle occlusion by ischemia for 45 min, followed by 60 mins of reperfusion with contralateral nephrectomy in rats. The rats were pretreated intraperitoneally with a quercetin suspension (50 mg/kg) 60 min before the ischemia induction. Thiobarbituric acid reactive substances (TBARS), protein carbonyl content, tumor necrosis factor alpha (TNF-alpha), reduced glutathione (GSH) levels, myeloperoxidase (MPO) catalase (CAT) and superoxide dismutase (SOD) activities were determined in renal tissue. RESULTS: There were 3 groups of rats, the control group, the I/R group and the I/R+Q group. Our results indicate that TBARS, TNF-alpha levels, MPO activity and protein carbonyl content were significantly higher in the I/R group than those in the control group (p<0.05, p<0.01, p<0.01 and p<0.01, respectively). Quercetin administration significantly decreased these parameters (p<0.05, p<0.01, p<0.05 and p<0.01, respectively). GSH levels, SOD, and CAT activities significantly decreased after I/R injury when compared to the control group (p<0.01, p<0.05 and p<0.01, respectively). Quercetin treatment significantly increased GSH levels and activities of these enzymes when compared to the I/R group (p<0.05, p<0.01, p<0.05, respectively). CONCLUSIONS: These results suggest that quercetin reduces renal oxidative injury and facilitates repair. Quercetin can have a role in a renoprotective therapeutic regimen.

Quercetin reduces cisplatin nephrotoxicity in rats without compromising its antitumour activity
1. 2. 3. 4. 5. Penelope D. Sanchez-Gonzalez1,2, Francisco J. Lopez-Hernandez1,2,3, Fernando Perez-Barriocanal1,2, Ana I. Morales1,2 and Jose M. Lopez-Novoa1,2

+ Author Affiliations 1. Unidad de Fisiopatologa Renal y Cardiovascular, Departamento de Fisiologa y Farmacologa, Universidad de Salamanca, Salamanca, Spain 2. 2Instituto Reina Sofa de Investigacin Nefrolgica, Madrid, Spain 3. 3Unidad de Investigacin, Hospital Universitario de Salamanca, Salamanca, Spain 1. Correspondence and offprint requests to: Jose M. Lopez-Novoa; E-mail: jmlnovoa@usal.es

1

Received January 25, 2011. Accepted March 22, 2011.

Abstract
Background. Nephrotoxicity is the major limitation for the clinical use of cisplatin as an anti-tumoural drug. Our aim was to investigate the protective effect of quercetin on cisplatin nephrotoxicity in a rat tumour model in vivo and to examine the mechanisms of renal protection. Methods. Breast adenocarcinoma (13762 Mat B-III) cells were inoculated subcutaneously in male Fischer rats and 7 days later, the rats were administered daily with quercetin [50 mg/kg/day, intraperitoneally (i.p.)] or vehicle. Four days after that, the rats were given a single dose of cisplatin (4 mg/kg, i.p.) or vehicle. Tumour growth and renal function were monitored throughout the experiment. Two or 6 days after cisplatin administration, the rats were killed and the kidneys and tumours were removed to examine renal function and toxicity markers in both tissues. Results. In the kidney, cisplatin treatment induced: (i) a decrease in renal blood flow and glomerular filtration rate, (ii) tubular necrosis/apoptosis, (iii) increased lipid peroxidation and decreased endogenous antioxidant systems, (iv) increased expression of inflammation markers and (v) increased activity of the apoptosis executioner caspase-3. Cisplatin effectively reduced tumour size and weight. Conclusions. Co-treatment with quercetin partially prevented all the renal effects of cisplatin, whereas it did not impair its anti-tumour activity. In conclusion, in a model of tumour-bearing

rats, quercetin prevents the nephrotoxic effect of cisplatin without affecting its anti-tumour activity.

QUERCETIN, AN ANTI-OXIDANT BIOFLAVONOID, ATTENUATES DIABETIC NEPHROPATHY IN RATS


1. Muragundla Anjaneyulu, 2. Kanwaljit Chopra

Article first published online: 26 MAR 2004 DOI: 10.1111/j.1440-1681.2004.03982.x Issue

Clinical and Experimental Pharmacology and Physiology


Volume 31, Issue 4, pages 244248, April 2004 Additional Information(Show All) How to CiteAuthor InformationPublication History
How to Cite

Anjaneyulu, M. and Chopra, K. (2004), QUERCETIN, AN ANTI-OXIDANT BIOFLAVONOID, ATTENUATES DIABETIC NEPHROPATHY IN RATS. Clinical and Experimental Pharmacology and Physiology, 31: 244248. doi: 10.1111/j.14401681.2004.03982.x
Author Information

1. Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, India

*Correspondence: Dr Kanwaljit Chopra, Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh-160014, India. Email: Dr_chopra_k@yahoo.com
Publication History 1. Issue published online: 26 MAR 2004 2. Article first published online: 26 MAR 2004 3. Received 21 February 2003; revision 5 September 2003; accepted 4 January 2004.

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diabetic nephropathy; lipid peroxidation; oxidative stress; quercetin; renal functions; streptozotocin

SUMMARY

1. Diabetic nephropathy is an important microvascular complication and one of the main causes of end-stage renal disease. Many in vivo and in vitro studies have indicated that oxidative stress is one of the major pathophysiological mechanisms involved in the development of diabetic nephropathy. In the present study, we examined the effect of an antioxidant bioflavonoid quercetin on renal function and oxidative stress in streptozotocin (STZ)induced diabetic rats. 2. Diabetes was induced in Sprague-Dawley rats with a single intravenous injection of STZ (45 mg/kg). Four weeks after STZ injection, quercetin (10 mg/kg per day) was given orally for 4 weeks in both control and diabetic rats. Plasma glucose levels and bodyweights were measured at 4 and 8 weeks after the STZ injection. At the termination of the experiments, urine albumin excretion, urine output, serum creatinine, blood urea nitrogen, creatinine and urea clearance were measured. The renal oxidative stress marker malonaldehyde, glutathione levels and the anti-oxidant enzymes superoxide dismutase and catalase were measured in kidney homogenate. 3. Streptozotocin-injected rats showed significant increases in blood glucose, polyuria, proteinuria and a decrease in bodyweight compared with age-matched control rats. After 8 weeks, diabetic rats exhibited renal dysfunction, as evidenced by reduced creatinine and urea clearance, and proteinuria along with a marked increase in oxidative stress, as determined by lipid peroxidation and activities of key anti-oxidant enzymes. Treatment with quercetin significantly attenuated renal dysfunction and oxidative stress in diabetic rats. 4. These results confirm the role of oxidative stress in the development of diabetic nephropathy and point to the possible anti-oxidative mechanism being responsible for the nephroprotective action of quercetin.

National Kidney Foundation Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification
1. Andrew S. Levey, MD; 2. Josef Coresh, MD, PhD; 3. Ethan Balk, MD, MPH; 4. Annamaria T. Kausz, MD, MS; 5. Adeera Levin, MD; 6. Michael W. Steffes, MD, PhD; 7. Ronald J. Hogg, MD; 8. Ronald D. Perrone, MD; 9. Joseph Lau, MD; and 10. Garabed Eknoyan, MD + Author Affiliations 1. From Tufts-New England Medical Center and Tufts University School of Medicine, Boston, Massachusetts; Bloomberg School of Public Health, Welch Center for Prevention, Epidemiology and Clinical Research, and the Johns Hopkins University, Baltimore, Maryland; University of British Columbia, Vancouver, British Columbia, Canada; University of Minnesota, Minneapolis, Minnesota; North Texas Hospital for Children, Dallas, Texas; and Baylor College of Medicine, Houston, Texas. Next Section

Abstract
Chronic kidney disease is a worldwide public health problem with an increasing incidence and prevalence, poor outcomes, and high cost. Outcomes of chronic kidney disease include not only kidney failure but also complications of decreased kidney function and cardiovascular disease. Current evidence suggests that some of these adverse outcomes can be prevented or delayed by early detection and treatment. Unfortunately, chronic kidney disease is underdiagnosed and undertreated, in part as a result of lack of agreement on a definition and classification of its stages of progression. Recent clinical practice guidelines by the National Kidney Foundation 1) define chronic kidney disease and classify its stages, regardless of underlying cause, 2) evaluate laboratory measurements for the clinical assessment of kidney disease, 3) associate the level of kidney function with complications of chronic kidney disease, and 4) stratify the risk for loss of kidney function and development of cardiovascular disease. The guidelines were developed by using an approach based on the procedure outlined by the Agency for Healthcare Research and Quality.

This paper presents the definition and five-stage classification system of chronic kidney disease and summarizes the major recommendations on early detection in adults. Recommendations include identifying persons at increased risk (those with diabetes, those with hypertension, those with a family history of chronic kidney disease, those older than 60 years of age, or those with U.S. racial or ethnic minority status), detecting kidney damage by measuring the albumincreatinine ratio in untimed (spot) urine specimens, and estimating the glomerular filtration rate from serum creatinine measurements by using prediction equations. Because of the high prevalence of early stages of chronic kidney disease in the general population (approximately 11% of adults), this information is particularly important for general internists and specialists. Chronic kidney disease is a worldwide public health problem. In the United States, the incidence and prevalence of kidney failure are rising, the outcomes are poor, and the costs are high. The number of persons with kidney failure who are treated with dialysis and transplantation is projected to increase from 340 000 in 1999 to 651 000 in 2010 (1). The major outcomes of chronic kidney disease, regardless of cause, include progression to kidney failure, complications of decreased kidney function, and cardiovascular disease (CVD). Increasing evidence indicates that some of these adverse outcomes can be prevented or delayed by early detection and treatment (2). Unfortunately, chronic kidney disease is underdiagnosed and undertreated, resulting in lost opportunities for prevention (3-5), in part because of a lack of agreement on a definition and classification of stages in the progression of chronic kidney disease (6) and a lack of uniform application of simple tests for detection and evaluation. In February 2002, the Kidney Disease Outcomes Quality Initiative (K/DOQI) of the National Kidney Foundation (NKF) published 15 clinical practice guidelines on chronic kidney disease [7]. The goals of the guidelines are to 1) define chronic kidney disease and classify its stages, regardless of underlying cause; 2) evaluate laboratory measurements for the clinical assessment of kidney disease; 3) associate the level of kidney function with complications of chronic kidney disease; and 4) stratify the risk for loss of kidney function and development of CVD. Our goal is to disseminate the simple definition and five-stage classification system of chronic kidney disease, to summarize the major recommendations on early detection of chronic kidney disease in adults (Table 1), and to consider some of the issues associated with these recommendations. Because of the high prevalence of early stages of chronic kidney disease in the general population, this information is particularly important for general internists and specialists.

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