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Egyptian Journal of Basic and Clinical Pharmacology

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ejbcp: Vol. 11
Research Article
Egyptian Journal of Basic and Clinical Pharmacology
Vol. 11 (2021), Article ID 101497, 7 pages 
doi:10.32527/2021/101497

Hypolipidemic and Anti-Oxidant Effects of Curcumin in Dexamethasone-Induced Dyslipidemia in Rats

Walaa I. Mohammed

Department of Clinical Pharmacology, Faculty of Medicine, Sohag University, Egypt

Received 23 August 2020; Accepted 20 January 2021

Editor: Omnyah Aly Elkharashi

Copyright © 2021 Walaa I. Mohammed. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The present study investigated the hypolipidemic and anti-oxidant effects of curcumin in dexamethasone-induced dyslipidemia in rats. Rats classified into five groups, contained six animals each. All groups received their treatments daily for seven consecutive days. Control group: rats were injected subcutaneously with saline. Dexamethasone group: rats were injected subcutaneously with 10 mg/kg dexamethasone. Curcumin group: rats were injected subcutaneously with 10 mg/kg dexamethasone and concomitantly treated orally with 100 mg/kg curcumin. Atorvastatin group: rats were injected subcutaneously with 10 mg/kg dexamethasone and concomitantly treated orally with 10 mg/kg atorvastatin. Combination group: rats were injected subcutaneously with 10 mg/kg dexamethasone and concomitantly treated orally with a combination of 100 mg/kg curcumin and 10 mg/kg atorvastatin. At the end of the experiment, lipid profile, aspartate aminotransferase and alanine aminotransferase levels were measured in the serum. Malondialdehyde level and superoxide dismutase activity were measured in hepatic tissue. Besides, atherogenic index was estimated. The present study demonstrated that administration of curcumin significantly decreased serum levels of total cholesterol, total triglycerides, as well as decreased serum levels of low-density lipoprotein cholesterol compared to dexamethasone group. While, high-density lipoprotein cholesterol serum level was significantly increased compared to dexamethasone group. Moreover, atherogenic index was significantly decreased compared to dexamethasone group. Serum aspartate aminotransferase and alanine aminotransferase levels were significantly decreased compared to dexamethasone group. In addition, hepatic level of malondialdehyde was significantly decreased, while hepatic superoxide dismutase activity was significantly increased compared to dexamethasone group. These results suggested that curcumin has hypolipidemic and anti-oxidant effects in dexamethasone-induced dyslipidemia in rats.

1. Introduction

Hyperlipidemia participates markedly in the appearance and progression of atherosclerosis and coronary heart diseases. Atherosclerosis is an important disease responsible for the development of ischemic heart diseases, cerebrovascular diseases (CVD) and peripheral vascular diseases [1].

Dexamethasone is one of the long-acting synthetic steroids, used in the treatment of many inflammatory disorders. One of dexamethasone serious problems is "misuse" via uptake of an excessive dose [2]. Dexamethasone excessive dose produced hyperglycemia, hyperlipidemia, development of steatosis and fatty liver [3, 4]. In addition, many experimental studies showed that dexamethasone toxicity induced oxidative stress and increase malondialdehyde (MDA) level which is a significant indicator of lipid peroxidation [5,6,7].

Curcumin, a chief ingredient of turmeric, is recognized to posse anti-inflammatory and antioxidant effects in different diseases by scavenging reactive oxygen and nitrogen species and blocking lipid peroxidation. As well as, it promotes the biosynthesis of different cytoprotective and antioxidant proteins [8,9].

Several studies showing the ability of curcumin to decrease serum cholesterol and triglycerides levels [10,11,12], but its effect on dyslipidemia induced by dexamethasone not previously studied. So, this work was performed to investigate the hypolipidemic and anti-oxidant effects of curcumin in dexamethasone-induced dyslipidemia in rats. The lipid profile was investigated; serum total cholesterol (TC), total triglycerides (TGs), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C). Moreover, atherogenic index (AI) is used to assess the risk of development of atherogenicity in vessels. The liver is the main organ commonly affected by hyperlipidemia, therefore serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, were also investigated. As dexamethasone-induced dyslipidemia is linked to increased production of reactive oxygen species (ROS) and oxidative damage, hepatic MDA level and hepatic superoxide dismutase (SOD) activity were also measured.

2. Materials and Methods

2.1. Drugs

Curcumin was purchased from ALPH Globalsearch, India. Atorvastatin was obtained fromSigma-Aldrich (USA). Dexamethasone was obtained from AK Scientific, Inc. (USA).

2.2. Animals

Thirty male adult albino rats, with an average weight of "150-200 gm" were used in the experiment. Animals were obtained from the animal house, Faculty of Science, Sohag University, Egypt. The animals dwelled in the animal house, Faculty of Medicine, Sohag University, Egypt. The temperature was maintained at (25±2oC) with 12 hours day/night cycle. The experimental protocol was accepted by the Committee of Research Ethics, Faculty of Medicine, Sohag University, Egypt, (Approval No. IBR # S20-145).

2.3. Experimental study

Rats were acclimatized for one week and then were divided into five groups, each contained six animals. All groups received their treatments daily for seven consecutive days.

Control group: rats were injected subcutaneously with saline.

Dexamethasone group: rats were injected subcutaneously with 10 mg/kg dexamethasone dissolved in saline [6].

Curcumin group: rats were injected subcutaneously with 10 mg/kg dexamethasone and concomitantly treated orally with 100 mg/kg curcumin dissolved in the corn oil [13].

Atorvastatin group: rats were injected subcutaneously with 10 mg/kg dexamethasone and concomitantly treated orally with 10 mg/kg atorvastatin dissolved in distilled water [14].

Combination group: rats were injected subcutaneously with 10 mg/kg dexamethasone and concomitantly treated orally with a combination of 100 mg/kg curcumin and 10 mg/kg atorvastatin.

Twenty-four hours after the end of the experiment, all rats were fasted, and blood samples were collected through the retro-orbital sinus puncture and centrifugated at 3000 rpm for 10 minutes for serum separation. Serum TC, TGs and HDL-C levels were measured spectrophotometrically (analytik jena, Germany) using commercially available kits, Human Gesellschaft for Biochemica and Diagnostic mbH, Germany, and expressed in mg/dl. While serum LDL-C and atherogenic index were calculated. LDL-C = TC – TGs/5 – HDL-C [15]. Atherogenic index (AI) = TC – HDL-C / HDL-C [16]. Moreover, serum ALT and AST levels were measured spectrophotometrically (analytik jena, Germany) using standardized commercially available kits (Egyptian Company for Biotechnology, Cairo, Egypt, and expressed in U/L.

The investigated rats of all groups were then sacrificed by decapitation. Liver was dissected out and liver samples were used for measurement of hepatic MDA and SOD levels. The liver tissues from all groups were homogenized using motor-driven homogenizer in 5 ml cold potassium phosphate buffer, pH 7.4. The homogenates were centrifuged at 4000 rpm for 15 minutes at 4∘C. The supernatant was used for the assay of hepatic MDA and SOD levels using standardized commercially available kits (Bio-Diagnostic Company, Egypt).

Malondialdehyde level was measured by a colorimetric method according to Ohkawa et al. [17]. This assay based on the formation of a thiobarbituric acid reactive product during the reaction of thiobarbituric acid with malondialdehyde in an acidic medium at a temperature of 95∘C for 30 min. MDA level was expressed in nmol/g tissues.

Superoxide dismutase level was measured by a colorimetric method as described by Nishikimi et al. [18]. The method builds on the ability of the enzyme to inhibit the phenazine methosulphate-mediated reduction of nitroblue tetrazolium dye. SOD activity was expressed as U/g tissue.

2.4. Statistical analysis:

Data were analyses with SPSS statistical software (V. 22), and the results were presented as mean±standard error (SE). The significance (P<0.05) between studied groups was estimated by ANOVA followed by Tukey post hoc test.

3. Results

3.1. Changes of the lipid profile:

The obtained results in table (1) revealed that serum levels of TC, TGs and LDL-C were significantly (P<0.05) increased in the dexamethasone group compared to the control group. Daily oral treatment of the rats with 100 mg/kg curcumin for seven days concomitantly with daily dexamethasone subcutaneous injection produced significant (P<0.05) decrease in TC, TGs and LDL-C serum levels compared to dexamethasone group. Daily oral treatment of the rats with 10 mg/kg atorvastatin for seven days concomitantly with daily dexamethasone subcutaneous injection produced significant (P<0.05) decrease in TC, TGs and LDL-C serum levels compared to dexamethasone group. Moreover, rats treated orally with a combination of 100 mg/kg curcumin and 10 mg/kg atorvastatin daily for seven days concomitantly with daily dexamethasone subcutaneous injection produced significant (P<0.05) decrease in TC, TGs and LDL-C serum levels compared to dexamethasone group.

On the other hand, in dexamethasone group, HDL-C serum level was significantly (P<0.05) decrease in comparison with the control group, and daily oral treatment of the rats with 100 mg/kg curcumin "in curcumin group" significantly (P<0.05) increased its serum level compared to dexamethasone group. Furthermore, in the atorvastatin group, serum HDL-C level was significantly (P<0.05) increased in comparison with the dexamethasone group. Besides, the combination group showed significantly (P<0.05) increased HDL-C serum level in comparison with dexamethasone group.

Regarding the lipid profile, insignificant difference (P>0.05) between curcumin, atorvastatin and combination groups were observed.

3.2. Changes of the atherogenic index:

The atherogenic index of dexamethasone group was significantly (P<0.05) increased compared to control group. Treatment of rats with curcumin, atorvastatin or their combination significantly (P<0.05) decreased atherogenic index compared to dexamethasone group. There was statistically insignificant difference (P>0.05) between curcumin, atorvastatin and combination groups (Fig. 1).

T1

Table 1: Serum lipid profile values in dexamethasone- induced dyslipidemic rats treated orally with curcumin, atorvastatin and combination of both.

F1
Figure 1: Effect of oral administration of curcumin, atorvastatin and combination of both on atherogenic index of dexamethasone- induced dyslipidemic rats. Values presented as mean±SE, for 6 rats. Dex= dexamethasone, Curc = curcumin, Ator = atorvastatin, Comb = combination. *Significant compared to control. a Significant compared to dexamethasone group.
F2
Figure 2: Effect of oral administration of curcumin, atorvastatin and combination of both on serum ALT level of dexamethasone- induced dyslipidemic rats. Values presented as mean±SE, for 6 rats. Dex= dexamethasone, Curc = curcumin, Ator = atorvastatin, Comb = combination. *Significant compared to control. a Significant compared to dexamethasone group.
F3
Figure 3: Effect of oral administration of curcumin, atorvastatin and combination of both on serum AST level of dexamethasone- induced dyslipidemic rats. Values presented as mean±SE, for 6 rats. Dex= dexamethasone, Curc = curcumin, Ator = atorvastatin, Comb = combination. *Significant compared to control. a Significant compared to dexamethasone group.
F4
Figure 4: Effect of oral administration of curcumin, atorvastatin and combination of both on hepatic MDA level of dexamethasone- induced dyslipidemic rats. Values presented as mean±SE, for 6 rats. Dex= dexamethasone, Curc = curcumin, Ator = atorvastatin, Comb = combination. *Significant compared to control. a Significant compared to dexamethasone group. # Significant compared to Curc group. & Significant compared to Ator group.
F5
Figure 5: Effect of oral administration of curcumin, atorvastatin and combination of both on hepatic SOD level of dexamethasone- induced dyslipidemic rats. Values presented as mean±SE, for 6 rats. Dex= dexamethasone, Curc = curcumin, Ator = atorvastatin, Comb = combination. *Significant compared to control. a Significant compared to dexamethasone group.
3.3. Changes in ALT and AST levels:

As shown in Fig.2,3. Serum ALT and AST levels were significantly (P<0.05) increased in the dexamethasone group compared to the control group. Daily oral treatment of the rats for seven days with 100 mg/kg curcumin in the curcumin group, or with10 mg/kg atorvastatin in atorvastatin group or their combination in the combination group concomitantly with daily subcutaneous injection of 10 mg/kg dexamethasone exhibited significantly (P<0.05) decreased ALT and AST serum levels compared to dexamethasone group. insignificant difference (P>0.05) statistically present among curcumin, atorvastatin and combination groups.

3.4. Changes in hepatic MDA and SOD levels:

Dexamethasone group showed significantly (P<0.05) increased MDA level in hepatic tissue compared to the control group (Fig.4). whereas, rats treated with daily oral dose of 100 mg/kg curcumin or 10 mg/kg atorvastatin or the combination of both concomitant with 10 mg/kg dexamethasone subcutaneous injection led to decrease hepatic MDA level significantly (P<0.05) compared to dexamethasone group (Fig.4). Moreover, the combination group exhibited statistically significant (P<0.05) decrease in hepatic MDA level compared to both the curcumin group and the atorvastatin group (Fig.4).

Superoxide dismutase level in the hepatic tissues was significantly (P<0.05) decrease in the dexamethasone group compared to the control group (Fig.5). Besides, compared to the dexamethasone group, the results revealed a significantly (P<0.05) increased hepatic SOD in the curcumin group, the atorvastatin group and the combination group but with statistically (P>0.05) insignificant difference between them (Fig.5),

4. Discussion

This work demonstrated that daily subcutaneous injection of the rats with high dose dexamethasone (10 mg/kg) for seven successive days produced marked dyslipidemia as evidenced by the significant disturbance in the lipid profile when compared with the control group. Our results agree with the results of Dolatabadi and Mahboubi. [19]. Moreover, subcutaneous dexamethasone injection produced a significant increase in the atherogenic index, that may increase the risk of atherogenicity, compared to the control group. Dexamethasone is a potent synthetic glucocorticoid, it can cause dyslipidemia through various mechanisms. Dexamethasone decreases the activity of lipoprotein lipase and increases hepatic secretion of very low-density lipoprotein cholesterol (VLDL). In addition, it increases hepatic lipogenesis and the accumulation of triglyceride within the liver. Dexamethasone enhances VLDL formation by the intestine, decreases the activity of lecithin cholesterol acetyltransferase and increased free cholesterol level. Moreover, it can increase the lipolysis in adipose tissue, and increase circulating fatty acids. On the other hand, a high level of dexamethasone is associated with insulin resistance, hyperinsulinemia, and hyperglycemia which are also linked to dyslipidemia [20,21,22,23]. Also, dexamethasone-induced dyslipidemia is related to overproduction of ROS and oxidative damage [24].

In this work, daily oral treatment of the rats with either curcumin or atorvastatin or their combination significantly corrected the abnormal lipid profile and the elevated atherogenic index induced by dexamethasone administration. These results are in concurrence with other studies [10,11,12] and indicated the hypolipidemic effect of curcumin. This hypolipidemic effect of curcumin may be attributed to the activation of cholesterol 7-α-hydroxylase, the first reaction in cholesterol metabolism, consequently motivating the formation of bile acid from cholesterol, a major route for cholesterol metabolism [25]. Moreover, curcumin decreases the activity of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase so that, it decreases serum and liver levels of cholesterol, triglycerides and free fatty acid [26]. On the other hand, the increase in HDL-C by curcumin administration indicating that curcumin can carry cholesterol back to the liver to be broken down and flushed from the body [27].

This work demonstrated a remarkable rise in the serum activities of ALT and AST in the dexamethasone group when compared with the control group. These high liver enzymes levels are used biochemically to assess liver toxicity and their release in the blood indicated hepatocytes membrane damage as a result of dexamethasone. These results corroborate the results obtained by Hasona and Morsi and Wego et al. [7,28], and indicating the toxic effects of dexamethasone on the liver.

As mentioned above, dexamethasone increase lipid lipolysis which results in a massive release of fatty acids. This fatty acid accumulates in the liver and leads to hepatic steatosis and inflammation and produces significant increase in ALT and AST activities [28].

In this work, daily oral treatment of the rats with either curcumin or atorvastatin or combination of both seems to improve the altered hepatic damage as it significantly restored normal serum levels of ALT and AST enzymes, showing the ability of curcumin to preserve the cell membrane and regenerate the injured cells and thus reduce the release of ALT and AST from cell cytoplasm. This finding concurred with the results of Hussein et al. [29] who observed that the elevated ALT and AST levels induced by the thioacetamide administration were significantly reduced by administration of curcumin.

Reactive oxygen species are responsible for the pathogenesis of cardiovascular disorders induced by glucocorticoid excess [30], and lipid peroxidation induced by ROS is a key factor for atherosclerosis [31]. In this work, a significant elevation in the lipid peroxides in the liver tissue during dexamethasone administration as expressed in MDA formation. Moreover, a significant decrease in the activity of the hepatic antioxidant enzyme, SOD was observed. These results coincide with Hasona et al. [3] who reported that extreme manufacture of free radicals because of oxidative stress is the main result of liver toxicity produced by dexamethasone.

Daily oral treatment of the rats with either curcumin or atorvastatin or their combination attenuated the MDA formation significantly and show a tendency to restore the normal SOD activity. These results harmonic with Abdelhamid et al. [32] and confirm the antioxidant effect of curcumin. On the other hand, a study of Arafa [11] showed that curcumin has no effect on the hepatic GSH and SOD levels and hypothesized that the hypolipidemic effects of curcumin are not related to its antioxidant effect. Curcumin inhibits ROS production and stimulates endogenic antioxidant efficacy by its free radical scavenging characteristics [33] due to its distinctive binding structure which explains its antioxidant activity. This antioxidant effect due to its two methoxylated phenols and an enol form of β- diketone acting as a radical-trapping for breaking lipid peroxidation chain reaction [34]. Moreover, the combination of curcumin with atorvastatin showed a more inhibitory effect on the MDA formation.

In conclusion, the results confirm that oxidative stress does a major role in dyslipidemia induced by dexamethasone. Administration of curcumin produced hypolipidemic and anti-oxidant effects in dexamethasone-induced dyslipidemia. Moreover, a combination of curcumin with atorvastatin seemed to be more beneficial as it produced a significant decrease in MDA level.

5. Funding

No funding resources.

6. Competing Interests

The author declares no competing interests.

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Research Article
Egyptian Journal of Basic and Clinical Pharmacology
Vol. 11 (2021), Article ID 101497, 7 pages 
doi:10.32527/2021/101497

Hypolipidemic and Anti-Oxidant Effects of Curcumin in Dexamethasone-Induced Dyslipidemia in Rats

Walaa I. Mohammed

Department of Clinical Pharmacology, Faculty of Medicine, Sohag University, Egypt

Received 23 August 2020; Accepted 20 January 2021

Editor: Omnyah Aly Elkharashi

Copyright © 2021 Walaa I. Mohammed. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The present study investigated the hypolipidemic and anti-oxidant effects of curcumin in dexamethasone-induced dyslipidemia in rats. Rats classified into five groups, contained six animals each. All groups received their treatments daily for seven consecutive days. Control group: rats were injected subcutaneously with saline. Dexamethasone group: rats were injected subcutaneously with 10 mg/kg dexamethasone. Curcumin group: rats were injected subcutaneously with 10 mg/kg dexamethasone and concomitantly treated orally with 100 mg/kg curcumin. Atorvastatin group: rats were injected subcutaneously with 10 mg/kg dexamethasone and concomitantly treated orally with 10 mg/kg atorvastatin. Combination group: rats were injected subcutaneously with 10 mg/kg dexamethasone and concomitantly treated orally with a combination of 100 mg/kg curcumin and 10 mg/kg atorvastatin. At the end of the experiment, lipid profile, aspartate aminotransferase and alanine aminotransferase levels were measured in the serum. Malondialdehyde level and superoxide dismutase activity were measured in hepatic tissue. Besides, atherogenic index was estimated. The present study demonstrated that administration of curcumin significantly decreased serum levels of total cholesterol, total triglycerides, as well as decreased serum levels of low-density lipoprotein cholesterol compared to dexamethasone group. While, high-density lipoprotein cholesterol serum level was significantly increased compared to dexamethasone group. Moreover, atherogenic index was significantly decreased compared to dexamethasone group. Serum aspartate aminotransferase and alanine aminotransferase levels were significantly decreased compared to dexamethasone group. In addition, hepatic level of malondialdehyde was significantly decreased, while hepatic superoxide dismutase activity was significantly increased compared to dexamethasone group. These results suggested that curcumin has hypolipidemic and anti-oxidant effects in dexamethasone-induced dyslipidemia in rats.

Research Article
Egyptian Journal of Basic and Clinical Pharmacology
Vol. 11 (2021), Article ID 101497, 7 pages 
doi:10.32527/2021/101497

Hypolipidemic and Anti-Oxidant Effects of Curcumin in Dexamethasone-Induced Dyslipidemia in Rats

Walaa I. Mohammed

Department of Clinical Pharmacology, Faculty of Medicine, Sohag University, Egypt

Received 23 August 2020; Accepted 20 January 2021

Editor: Omnyah Aly Elkharashi

Copyright © 2021 Walaa I. Mohammed. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

How to cite this article

Walaa I. Mohammed, "Hypolipidemic and Anti-Oxidant Effects of Curcumin in Dexamethasone-Induced Dyslipidemia in Rats," Egyptian Journal of Basic and Clinical Pharmacology, Vol. 11, Article ID 101497, 8 pages, 2020. doi:10.32527/2021/101497..

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