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Year : 2014  |  Volume : 4  |  Issue : 1  |  Page : 58-63

Role of chrysin on hepatic and renal activities of Nω-nitro-l-arginine-methylester induced hypertensive rats

Department of Biochemistry, Rajah Serfoji Government College, Thanjavur, Tamil Nadu, India

Date of Submission24-Aug-2013
Date of Acceptance02-Oct-2013
Date of Web Publication8-Jan-2014

Correspondence Address:
Malarvili Thekkumalai
Department of Biochemistry, Rajah Serfoji Government College, Thanjavur - 613 001, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2231-0738.124615

Clinical trial registration ijnpnd_75_13

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Objectives: The present study was undertaken to assess the antihypertensive, anti-hepatic and anti-renal activity of chrysin on Nω-nitro-l-arginine methyl ester (l-NAME) induced hypertensive rats. Materials and Methods: Hypertension was induced in adult male albino rats of the Wistar strain, weighing 180-220 g, by oral administration of the l-NAME (40 mg/kg B.W/day) in drinking water for 4 weeks. Rats were treated with chrysin (25 mg/kg B.W/day) for 4 weeks. Results and Discussion: Hypertension was manifested by considerably increased systolic and diastolic blood pressure and the toxic effect of 1-NAME was determined using the hepatic markers of lactate dehydrogenase, gamma glutamyl transpeptidase, renal markers of serum creatinine, creatinine clearance, urea, uric acid levels, urinary arachidonic acid metabolites of 6-keto-prostaglandin F 1α, thromboxane B2, 8-isoprostane-prostaglandin F and inflammatory parameters interleukin-6, tumor necrosis factor-alpha. Supplementation of chrysin at the dosage of 25 mg/kg considerably decreased systolic and diastolic blood pressure, hepatic markers, renal markers, urinary arachidonic acid metabolites and inflammatory parameters. Conclusion: These results suggest that chrysin decreases the blood pressure, significantly restores hepatic marker, renal markers, urinary arachidonic acid metabolites and inflammatory parameters and thus exhibits antihypertensive and anti-renal effects in l-NAME induced hypertensive rats.

Keywords: Glutamyl transpeptidase, interleukin, nitric oxide, thromboxane B2

How to cite this article:
Ramanathan V, Thekkumalai M. Role of chrysin on hepatic and renal activities of Nω-nitro-l-arginine-methylester induced hypertensive rats. Int J Nutr Pharmacol Neurol Dis 2014;4:58-63

How to cite this URL:
Ramanathan V, Thekkumalai M. Role of chrysin on hepatic and renal activities of Nω-nitro-l-arginine-methylester induced hypertensive rats. Int J Nutr Pharmacol Neurol Dis [serial online] 2014 [cited 2022 Aug 17];4:58-63. Available from:

   Introduction Top

Hypertension is a major risk factor for cardiovascular mortality and morbidity, through its effects on target organs such as the heart, liver and kidney. [1] At the moment, hypertension afflicts more than 1 billion adults world-wide and 90-95% of these patients have essential hypertension. [2] Hypertension and its related developments such as coronary artery disease, stroke, heart failure and chronic kidney disease is a growing public health problem for which successful treatment often remains inadequate. [3] Hypertension is mainly attributable to endothelial dysfunction, which results from nitric oxide (NO) deficiency. In fact, it has been found that vascular endothelium of hypertensive patients produces less NO, a key regulator of the cardiovascular system and metabolic homeostasis. [4] NO is recognized as the endothelium-derived relaxing factor responsible for vascular dilation. Moreover, NO is known to be an anti-hypertrophic agent. [5] Nω-nitro-l-arginine methylester (l-NAME) is a non-specific inhibitor of all nitric oxide synthase (NOS) including neuronal nitric oxide synthase, inducible nitric oxide synthase and endothelial nitric oxide synthase. Supplementation of l-NAME can induce high blood pressure in animal models. [6] l-NAME-induced hypertension is thus a suitable model to study the cardiovascular effects of new active substances. The kidney is one of the organs targeted by hypertension. Renal disease secondary to hypertension progressively develops, culminating in chronic renal failure with a loss of glomeruli and several lots of morphological features and accompanying quantitative alterations. [7]

Flavonoids are usually plant polyphenolic compounds that consist of a number of classes, including flavanols, flavones and flavans. Chrysin (5,7-dihydroxy flavones [Figure 1] is a naturally occurring flavone contained in flowers such as the blue passion flower (Passiflora caerulea) and the Indian trumpet flower, as well as in edible items such as mushroom, [8] honey and propolis. [9] Chrysin has been found to possess antioxidant, [10] anti-allergic, [11] anti-inflammatory, [12] anti-cancer, [13] antiestrogenic, [14] anxiolytic [15] and antihypertension [16] properties.
Figure 1: Chemical structure of chrysin (5,7 dihydroxyfl avone)

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The prospective adverse reactions of chrysin have not been well studied. Only limited studies have been carried out to investigate its antioxidant properties and its role as an antihypertensive agent. The present study was indicate to know the association between hepatic markers of lactate dehydrogenase (LDH), gamma glutamyl transpeptidase (GGT), renal markers of serum creatinine, creatinine clearance, urea, uric acid (UA) levels, 8-isoprostane-prostaglandin F(8-iso-PGF), 6-keto-prostaglandin F(6-keto-PGF) , thromboxane B2 (TXB2) and Inflammatory parameters interleukin-6 (Il-6), tumor necrosis factor-alpha (TNF-α) in l-NAME induced hypertensive rats.

   Materials and Methods Top


Chrysin and l-NAME was purchased from Sigma Chemical Co. (St. Louis, MO, USA). All other chemicals used in this study were of analytical grade and obtained from E-Merck or HIMEDIA, Mumbai, India.


All the animal handling and experimental procedures were approved by the Institutional Animal Ethics Committee of Bharathidasan University (Registration no: 418/01/a/date 04.06.2001) and animals were cared for in accordance with the Indian National Law on Animal Care and Use. Male Wistar rats (180-220 g) were purchased from the Indian Institute of Science, Bangalore, India. Rats were housed in plastic cages with filter tops under controlled conditions of a 12 h light-dark cycle, 50% humidity and temperature of 28°C. All rats received a standard pellet diet (Lipton Lever Mumbai, India) and water ad libitum (BDU/IAEC63/2013).

Induction of l-NAME-induced hypertension

l-NAME (40 mg/kg B.W) was dissolved in drinking water and given to rats at an interval of 24 h for 8 weeks. Mean arterial blood pressure (MAP) was measured using tail cuff method. MAP measurements were performed at the time of 1-8 weeks.

Study design

Animals were divided into four groups of six rats each and all were fed the standard pellet diet. The rats were grouped as given below.

  • Group I : Control
  • Group II : Normal + chrysin (25 mg/kg of B.W) after 4 th week
  • Group III : l-NAME induced hypertension (40 mg/kg of B.W)
  • Group IV : l-NAME induced hypertension + Chrysin (25 mg/kg of B.W).

Chrysin was administered orally once in a day in the morning for 4 weeks. The compound was suspended in 2% dimethyl sulfoxide solution and fed by intubation. After the 8 th week morning, the animals were sacrificed by cervical dislocation. The blood was collected in clean dry test tubes and allowed to coagulate at ambient temperature for 30 minutes. Serum was separated by centrifugation at 2000 rpm for 10 minutes. The blood, collected in a heparinized centrifuge tube, was centrifuged at 2000 rpm for 10 minutes and the plasma separated by aspiration was used for estimations.

Experimental methods

The serum GGT; EC was assayed according to the method of Rosalki and Rau. [17] The activity of LDH; EC was estimated by the method of King. [18] The serum urea, UA and creatinine, creatinine clearance were estimated by using diagnostic kits based on the methods of Fawcett and Scott, [19] Caraway [20] and Jaffe [21] respectively. Urinary 6-keto-PGF, TXB2, 8-iso-PGF2α, Il-6 and TNF-α were assayed according to the general principles of the enzyme-linked immunosorbant assay technique [22] using specific and sensitive kits (Cayman Chemical, Ann Arbor, MI, USA).

Statistical analysis

Data were analyzed by one-way analysis of variance followed by a Duncan's multiple range tests using a commercially available statistics software package (SPSS for Windows, version 11.0; SPSS Inc., Chicago, IL, USA). Results were presented as mean ± standard deviation (SD) values of P < 0.05 were regarded as statistically significant.

   Results Top

[Table 1] shows the activities of hepatic and renal functional markers such as GGT, LDH, creatinine, cratinine clearance, urea and UA in control and l-NAME induced hypertensive rats. The activities of these markers were increased significantly in l-NAME induced hypertensive rats and administration of chrysin significantly decreased the activities of these markers.
Table 1: Effect of chrysin on hepatic markers and renal markers in serum

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Urinary arachidonic acid metabolites such as 6-keto-PGF were slightly higher (P < 0.05), and the excretion of TXB2 and 8-iso-PGF was more pronounced (P < 0.05 respectively) as despicted in [Table 2]. Supplementation of chrysin significantly reduced the 6-keto-PGF , TXB2 and 8-iso-PGF compared to untreated l-NAME induced hypertensive rats.

[Table 3] shows elevated serum levels of Il-6 and TNF-α in l-NAME induced hypertensive rats (Group III) when compared to control. Supplementation of chrysin in (Group IV) reduced serum levels of Il-6 and TNF-α compared to l-NAME induced hypertensive rats. There is no significant variance between the control (Group I) and chrysin supplementation of the control (Group II).
Table 2: Effect of chrysin on urinary arachidonic acid metabolites of 6-keto-PGF1á, TXB2 and 8-iso-PGF2á

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Table 3: Effect of chrysin on infl ammatory parameters of IL-6 and TNF-á

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   Discussion Top

Serum GGT and LDH are membrane bound enzymes, which may be secreted unequally depending on the pathological phenomenon. LDH is a cytosolic enzyme, which exists in all the tissues involved in glycolysis and prevails in five different isoforms specific as LDH1-LDH5. [23] GGT and LDH is excreted by the liver through bile and hence when liver is damaged, the serum enzyme level increases due to defective excretion. In our study, the action of GGT and LDH in the serum significantly increased in l-NAME induced hypertensive rats. The increase in the activities of GGT and LDH enzymes in the serum and pursuing fall in the tissue might be due to the leak of these cytosolic enzymes into the circulatory system resulting from liver as well as renal damage during l-NAME induced hypertensive rats. It is a measure of the renal as well as hepato-cellular damage due to kidney and liver dysfunction and disturbance in the biosynthesis of these enzymes, with alteration in the membrane permeability. Administration of chrysin prevented l-NAME induced renal toxicity and hepatotoxicity as indicated by as precipitous drop in serum GGT, LDH, creatinine and creatinine clearence levels, possibly by maintaining the integrity or renal cellular and hepato-cellular membrane. This is an indicator of possible nephro- and hepato-protective efficacy offered by chrysin.

Urea could be major nitrogen containing metabolic compound of necessary for protein metabolism; UA is the major product of purine nucleotides; creatinine is endogenously produced and released into body fluids and its clearance is a measure of the glomerular filtration rate. [24] The outcomes from the existing research reveal that l-NAME induced hypertensive rats show significantly increased levels of urea, UA and creatinine in serum as shown in earlier findings. [25] In addition to dyslipidemia, hypertensive rats suffered renal damages as evidenced by the elevation in serum urea and creatinine levels. [26] This is explained which there seemed to be clearance of blood urea and creatinine by the kidney, serum or even which right now there in which lowered necessary protein degradation.

UA could be the end product of endogenous as well as dietary purine nucleotide metabolism in humans. A growing body of data suggests a putative pathogenetic role for hyperuricemia in atherosclerosis and cardiovascular disease, especially in patients with diabetes mellitus, heart failure and hypertension. [27] Prospective studies have confirmed separate and important organizational associations of increased UA levels and cardiovascular events. [28] As regards blood pressure, elevated levels of UA have been identified as a forecaster of hypertension incidence and progression. [29] In the present study, serious self-consciousness of NOS by l-NAME caused an increase in serum urea UA level. Serum urea and UA is a sensitive and reliable biochemical index for evaluation of renal function in an animal model. The increased serum urea and UA indicates impairment of kidney function. Hypertensive rats also presented renal damages that were evidenced by the elevation in serum urea, UA, creatinine and creatinine clearance levels, which are considered as significant markers of renal dysfunction. Supplementation of chrysin prevented the increase in the levels of serum urea, UA, creatinine and creatinine clearance levels in l-NAME -induced hypertensive treated rats. This may due to chrysin having antireanl damage activity.

Arachidonic acid metabolites, a potent vasoconstrictor acting through TXA receptor activation, has been recommended as a paying attention of oxidative stress. [30] Urinary levels of 6-keto-PGF only increased a little bit, in line with the results of Tomida et al., [31] indicating that in l-NAME-hypertensive rats the levels of cyclooxygenase-2 (COX-2) messenger ribonucleic acid and necessary protein were increased in the kidneys and the thoracic aorta, suggesting that an increase in COX-2 expression might have a hypertensive effect partly associated with 8-iso-PGF formation in l-NAME rats. The present study shows supplementation of chrysin reduces the, TXB2, 6-keto-PGF and 8-iso-PGF in l-NAME induced hypertensive rats. The l-NAME induced group developed hypertension after the end of the first induction week. At the end of the experiment, an increase in inflammatory parameters (the serum Il-6 and TNF-α levels).

Il-6 is a pleiotropic cytokine having an array of biologic routines in immune regulation, hematopoiesis, inflammation and oncogenesis. Recent evidence indicates a pathological role for Il-6 in promoting proliferation of both smooth muscle and endothelial cells in the pulmonary arterioles, resulting in development of pulmonary arterial hypertension. [32] Biochemical markers, especially markers of vascular inflammation, such as high-sensitivity C-reactive protein (hs-CRP), have been recommended to be predictive of cardiovascular events. [33] The primary proinflammatory cytokines TNF-α and Il-6 include the major inducers of hs-CRP. On top of that, according to Navarro and Mora-Fernαndez, [34] TNF-α and Il-6 are regarded as causative of direct renal effects. In this particular study, treatment with chrysin reduced the serum Il-6 and TNF-α level. Experimental and clinical studies have demonstrated the pathogenic role of TNF-α in the development of renal injury and the potential benefit of modulating TNF-α activity as a therapeutic target in diverse renal diseases. Il-6 has been correlated with an increased width of the glomerular basement membrane. [35] It also enhances fibronectin expression, affects extracellular matrix dynamics at both the mesangial and podocyte levels, stimulates mesangial cell proliferation, and increases endothelial permeability. [36] Il-6 plays an important role in vascular remodeling and has been reported to be a useful biomarker in predicting cardiovascular events.

TNF-α is cytotoxic to glomerular, mesangial and epithelial cells, and it is able to induce direct renal damage. In addition, TNF-α stimulates endothelial generation of reactive oxygen species by activating the nicotinamide adenine dinucleotide phosphate-oxidase subunits gp91phox, NOX-1, p47phox, and p22phox. TNF-α also activates the transcription of nuclear factor-kappaB, which regulates the expression of genes involved in inflammation, oxidative stress and endothelial dysfunction. [37] Chrysin appears to alleviate adverse effects in l-NAME induced hypertensive rats by enhancing hepatic and inflammatory markers.

   Conclusion Top

Chrysin prevented progression of hypertension in rats produced by administration of l-NAME, which may be due to its diuretic, nephroprotective, antihyperlipidaemic and antioxidant effects. It can be concluded that the chrysin possesses strong antihypertensive properties in l-NAME induced hypertensive rats as evidenced by a significant decrease in the hepatic, renal markers, urinary arachidonic acid metabolites and inflammatory markers.

   References Top

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  [Figure 1]

  [Table 1], [Table 2], [Table 3]

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