Inflammopharmacology

, Volume 18, Issue 6, pp 309–315 | Cite as

Antihypercholesterolaemic effect of ginger rhizome (Zingiber officinale) in rats

  • El-Sayed M. ElRokh
  • Nemat A. Z. Yassin
  • Siham M. A. El-Shenawy
  • Bassant M. M. Ibrahim
Research Article

Abstract

Introduction

Many herbal medicinal products have potential hypocholesterolaemic activity and encouraging safety profiles. However, only a limited amount of clinical research exists to support their efficacy.

Aim of the work

The present study was designed to evaluate the antihypercholesterolaemic effects of aqueous ginger (Zingiber officinale) infusion in hypercholesterolaemic rat models.

Methods

48 rats were used throughout the experiment, which were divided into six groups, eight animals each as follows: normal control group (normal rats which fed with standard diet). After induction of hypercholesterolaemia by feeding rats with high cholesterol diet, the remaining rats were divided into five groups: group 1, hypercholesterolaemic control group (hypercholesterolaemic rats group); groups 2, 3 and 4, rats were given aqueous infusion of ginger (100, 200 and 400 mg/kg, respectively) orally; and group 5, rats were given atorvastatin (0.18 mg/kg) orally as a reference antihypercholesterolaemic drug. The blood was obtained from all groups of rats after being lightly anaesthetized with ether and the following lipid profile [serum total cholesterol (TC), HDL-cholesterol (HDL-C), LDL-C and triglyceride levels] was measured at zero time and 2 and 4 weeks after ginger and atorvastatin treatment, and the risk ratio (TC/HDL-cholesterol) was assessed.

Results

The results revealed that the hypercholesterolaemic rats treated with aqueous ginger infusion in the three doses used after 2 and 4 weeks of treatment induce significant decrease in all lipid profile parameters which were measured and improved the risk ratio.

Keywords

Zingiber officinale Hypocholesterolaemic Atorvastatin Lipid profile Rats 

Introduction

Hypercholesterolaemia means high cholesterol levels in the blood. It is not a disease but a metabolic disorder that can be secondary to many diseases and can contribute to many forms of disease, most notably cardiovascular disease. Elevated cholesterol does not lead to specific symptoms unless it has been longstanding. Some types of hypercholesterolaemia lead to specific physical findings: xanthoma (deposition of cholesterol in patches on the skin or in tendons), xanthelasma palpebrarum (yellowish patches around the eyelids) and arcus senilis (white discoloration of the peripheral cornea). Longstanding elevated hypercholesterolaemia leads to accelerated atherosclerosis; this can express itself in a number of cardiovascular diseases: coronary artery disease (angina pectoris, heart attacks), stroke and short stroke-like episodes and peripheral vascular disease (Durrington 2003). These conditions account for the majority of morbidity and mortality among middle-aged and older adults. The incidence of disease will increase over the next decade because of the epidemicity of obesity and aging. Both genetic disorders and life style including sedentary behavior and diets high in calories, saturated fats and cholesterol contribute to dyslipidemia. In atherosclerosis, the plaque blocks the artery and with time it can completely obstruct the artery (Samra 2001). High cholesterol levels are treated with diets low in cholesterol, medications, and rarely with other treatments including surgery (for particular severe subtypes). Medications include statins (most prominently rosuvastatin, atorvastatin, simvastatin, or pravastatin), cholesterol absorption inhibitors (ezetimibe), fibrates (gemfibrozil, bezafibrate, fenofibrate or ciprofibrate), vitamin B3 (niacin), bile acid sequestrants (colestipol, cholestyramine), LDL apheresis and in hereditary severe cases liver transplantation (Durrington 2003). Plant-derived products have been used for medicinal purposes for centuries. At present, it is estimated that about 80% of the world population relies on botanical preparations as medicines to meet their health needs. Herbs and spices are generally considered safe and proved to be effective against certain disease. They are also extensively used, particularly, in many Asian and African countries. Spices and herbs are widely used in phytotherapy, which is using plants and their chemical constituents to treat certain health problems. Researchers have been focused on various herbs that possess hypolipidemic properties which may be useful adjuncts in reducing the risk of coronary artery disease (Gardia et al. 1990) with the current drug medication used such as roots of aswagandha (Withania somnifera, Dunal) (Budhiraja and Sudhir 1987), leaves of mulberry (Morus indica L.) (Watanabe 1958) and the rhizomes of ginger (Zingiber officinale Rosc.) (Elam et al. 2000). Ginger belongs to Zingiberaceae family, the part of the plant used is rhizome, its Latin name is Zingiber (Govindarajan 1982). The ginger has been listed in “Generally Recognized as Safe” (GRAS) document of the US FDA (Langner et al. 1998). The fresh ginger rhizome contains polyphenolic compounds such as gingerols (6-gingerol, 8-gingerol); zingerone, which is the major active component (Gruenwald et al. 2000); and gingerol [5-hydroxy-1-(4-hydroxy-3-methoxy phenyl)decan-3-one is one of the most abundant constituents in the gingerol series and also responsible for its characteristic pungent taste; Ney et al. 1988]. The aim of the present study is to evaluate the antihypercholesterolaemic effect of ginger (Z. officinale) in rat models of hypercholesterolaemia. In traditional Indian medicine or Ayurveda, ginger (from the rhizomes of Z. officinale Roscoe) has been used for medicinal purpose for the treatment of a number of diseases including those affecting the digestive tract (Afshari et al. 2007). Ginger is a household remedy for dyspepsia, flatulence, colic, diarrhoea and is used as a carminative (Langner et al. 1998).

The aim of the present study is to evaluate the antihypercholesterolaemic effect of ginger (Z. officinale) in rat models of hypercholesterolaemia.

Materials and methods

Materials

For the preparation of aqueous ginger infusion, 3 g of ginger powder was dissolved in 100 mL hot-distilled water and left until it was used.

Animals

Sprague-Dawley rats weighing 175–200 g, purchased from the animal house of National Research Centre, were used. The animals were housed in standard metal cages in an air-conditioned room at 22 ± 3°C, 55 ± 5% humidity, and 12-h light and provided with standard laboratory diet and water ad libitum. All animal experiment procedures were performed in accordance with the Ethics Committee of the National Research Centre and followed the recommendations of the National Institutes of Health Guide for Care and Use of Laboratory Animals (Publication No. 85-23, revised 1985).

Drugs and chemicals

  • Ginger powder was purchased from Mepaco Company for Pharmaceutical Industries, Egypt, dissolved in water in the form of aqueous ginger infusion and the dose used is 200 mg/kg according to Bhandari et al. (2005) and its half is 100 mg/kg and double of it is 400 mg/kg.

  • Atorvastatin was obtained from Unipharma Company for Pharmaceutical Industries, Egypt; the dose used was 0.18 mg/kg which was equivalent to maximum therapeutic human dose calculated as rodent dose equivalent of human therapeutic dose according to Paget and Barnes (1964).

  • Cholesterol powder, cholic acid and bile salts were obtained from Sigma.

  • Animal fats.

Diagnostic kits

Enzymatic colorimetric kits were used for the determination of lipid profile:
  • Total cholesterol according to Flegg (1973).

  • Triglycerides according to Wahlefeld (1974).

  • High-density lipoprotein cholesterol (HDL-C) according to Freidwald et al. (1972).

  • Low-density lipoprotein cholesterol (LDL-C) according to Wieland and Seidel (1983).

All kits used were commercially available and were obtained from Biodiagnostic Company.

Methodology

Forty-eight rats were used throughout the experiment, which were divided into six groups, eight animals each as follows: normal control group (normal rats which fed with standard diet). Hypercholesterolaemic group was induced by feeding the rats with high cholesterol diet by adding 1% cholesterol powder C27H46O + 0.2% cholic acid + 10% fat to the rat chow daily for 8 weeks before starting treatment and throughout the experiment (4 weeks); this group was divided into five groups: first group served as hypercholesterolaemic control group; second treated with atorvastatin (0.18 mg/kg) orally; groups 3, 4, 5 received 100, 200 and 400 mg/kg aqueous ginger infusion orally for 4 weeks. All groups continued to receive high cholesterol diet throughout the experiment (4 weeks).

Determination of lipid profile

Blood was obtained from the retro-orbital plexus of veins of all rat groups after overnight fasting after being lightly anaesthetized with ether before treatment (zero time) and 2 and 4 weeks (after treatment) of experiment. The blood was allowed to flow into clean dry centrifuge tube and left to stand for 30 min before centrifugation to avoid hemolysis. Samples were centrifuged for 15 min at 2,500 rpm. The clear supernatant, serum was separated and collected by Pasteur pipette into a dry clean tube for the following biochemical tests (lipid profile: total cholesterol, triglycerides, HDL-cholesterol and LDL-cholesterol.

Percentage of efficacy of aqueous ginger infusion in reducing risk ratio was calculated as percentage of change as compared with atorvastatin.

Risk ratio was calculated as the ratio between TC and HDL-C (TC/HDL-C), for men an acceptable ratio of TC/HDL is 4.5 or below, and for women is 4.0 or below (Gimeno-Orna et al. 2005).

Statistical analysis

Values were expressed as mean ± SE. Results were analyzed using one-way analysis of variance (ANOVA) followed by Bonferroni multiple comparisons test to compare all groups.

Results

The rats given aqueous ginger infusion orally at dose of 100, 200 and 400 mg/kg showed a significant reduction in the serum cholesterol level by 63.72, 60.78, 59.41% and by 70.85, 69.41, 77.46% after 2 and 4 weeks of treatment, respectively. While rats given atorvastatin orally in a dose of 0.18 mg/kg as a standard reference, hypolipidemic drug exhibited reduction in serum cholesterol level by 51.04 and 69.04% after 2 and 4 weeks of treatment, respectively (Table 1). The percentage effect of aqueous ginger infusion treatment is 124.85, 119.08, and 116.39% and 102.61, 100.53, and 112.92% after 2 and 4 weeks, respectively, as compared with atorvastatin group. Serum triglyceride levels in rats given ginger extract orally at the same dose mentioned above showed a significant reduction in serum triglyceride levels by 34.01, 73.6, and 74.76% and by 42.53, 84.28, and 90.49%, respectively, after 2 and 4 weeks of treatment, while rats treated with atorvastatin (0.18 mg/kg) exhibited a significant reduction in serum triglycerides by 43.41 and 76.79% after 2 and 4 weeks of treatment, respectively (Table 2). The percentage effect of aqueous ginger infusion (100, 200 and 400 mg/kg) treatment is 78.34, 169.68, and 172.21% and 55.38, 109.74, and 117.83%, respectively, after 2 and 4 weeks as compared with atorvastatin group. Rats treated with the ginger (100, 200 and 400 mg/kg) showed a significant reduction in serum LDL-C level by 92.31, 93.81, and 90.42% and by 96.48, 98.39, and 98.56% after 2 and 4 weeks of treatment, respectively. Rats treated with atorvastatin exhibited reduction in serum LDL-C by 85.05 and 85.96% after 2 and 4 weeks of treatment, respectively (Table 3). The percentage effect of aqueous ginger infusion treatment is 108.53, 110.29, and 106.31% and 112.23, 113.84, and 114.65% after 2 and 4 weeks of treatment, respectively, as compared with atorvastatin group. In contrast, rats treated with ginger (100, 200 and 400 mg/kg) showed increased percentage of HDL to total cholesterol level by 84.75, 88.67, and 82.64% and by 91.25, 94.96, and 95.17% after 2 and 4 weeks of treatment, respectively. Also, atorvastatin induced an increase by 77.6 and 66.7% after 2 and 4 weeks of treatment, respectively (Table 4). The percentage of serum HDL-C to total cholesterol was increased by 109.18, 114.24, and 106.46% and by 136.38, 142.23, and 142.55% after 2 and 4 weeks of ginger treatment, respectively, as compared with atorvastatin group. The risk ratio was decreased by 78.8 and 80.32%, 80.1 and 81.7%, and 82.53 and 84.71% after 2 and 4 weeks of ginger treatment (100, 200 and 400 mg/kg), respectively, while the risk ratio in the atorvastatin treated group was reduced by 75.8 and 71.83% after 2 and 4 weeks of treatment, respectively (Table 5). The percentage of effect of aqueous ginger infusion treatment in reducing risk ratio is 104.06, 105.6, and 108.83% and 111.79, 113.18, and 117.93%, respectively, after 2 and 4 weeks as compared with atorvastatin. The total cholesterol/HDL ratio is more indicative of cardiovascular disease than TC (total cholesterol). The amount of HDL and LDL in the blood is added together; this number for all practical purposes indicates the amount of total cholesterol. Therefore, if the HDL count is low, the LDL count will account for the remainder of the total. In the present work, the risk ratio was decreased in dose of 100 mg/kg by 78.8 and 80.32% after 2 and 4 weeks of treatment, respectively; dose 200 mg/kg reduced the risk ratio by 80.1 and 81.7% after 2 and 4 weeks of treatment, respectively, while dose of 400 mg/kg induced reduction by 82.53 and 84.71% after 2 and 4 weeks of treatment. In atorvastatin treated group, the risk ratio was reduced by 75.8 and 71.83% after 2 and 4 weeks of treatment (Table 5). The percentage of efficacy aqueous ginger infusion treatment in reducing risk ratio is 104.06, 105.6, and 108.83% and 111.79, 113.18, and 117.93% after 2 and 4 weeks, respectively, as compared with atorvastatin (more efficient than atorvastatin by 4.06, 5.6 and 8.83% after 2 weeks and by 11.79, 13.18, and 17.93% after 4 weeks, respectively).
Table 1

Effect of oral administration of aqueous ginger infusion (100, 200 and 400 mg/kg) and atorvastatin (0.18 mg/kg) in serum cholesterol level (mg/dL) after 2 and 4 weeks of treatment in hypercholesterolaemic rat model

Time

Normal control

Hypercholesterolaemic control

Ginger 100 mg/kg

Ginger 200 mg/kg

Ginger 400 mg/kg

Atorvastatin 0.18 mg/kg

Baseline before treatment

180.79 ± 1.31

385.86 ± 9.98*

244.75 ± 2.51*

263.97 ± 6.99*

283.12 ± 3.01*

240.66 ± 1.52*

2 weeks after treatment

172.81 ± 0.85

405.46 ± 11.31*

88.66 ± 3.18#

103.33 ± 4.04#

114.66 ± 4.58#

117.66 ± 6.11#

 % of change

↓3.84

↑4.78

↓63.72#,†

↓60.78#

↓59.41#

↓51.04#

4 weeks after treatment

178.99 ± 1.22

413.96 ± 6.35*

71.24 ± 2.8@

80.36 ± 1.57@

62.35 ± 1.9@

74.46 ± 1.18@

 % of change

↓0.45

↑6.82*

↓70.85@

↓69.41@

↓77.96@,†

↓69.04@

Data represent mean ± SE of each group (N = 8)

* Significance at P < 0.01 for all groups versus normal control group

#Significance at P < 0.01 for treated groups versus untreated hypercholesterolaemic control group after 2 weeks of treatment

@Significance at P < 0.01 for all treated groups versus untreated hypercholesterolaemic control group after 4 weeks of treatment

Significance at P < 0.01 for ginger group (100 mg/kg) after 2 weeks of treatment and ginger group (400 mg/kg) after 4 weeks of treatment versus atorvastatin

Table 2

Effect of oral administration of aqueous ginger infusion (100, 200 and 400 mg/kg) and atorvastatin (0.18 mg/kg) in serum triglyceride levels (mg/dL) after 2 and 4 weeks of treatment in hypertriglyceridemic rat model

Time

Normal control

Hypercholesterolaemic control

Ginger 100 mg/kg

Ginger 200 mg/kg

Ginger 400 mg/kg

Atorvastatin 0.18 mg/kg

Baseline before treatment

95.3 ± 2.6

177.16 ± 1.58*

114.47 ± 2.68*

135.53 ± 4.93*

158.04 ± 3.06*

118.33 ± 2.02*

2 weeks after treatment

87.67 ± 1.81

193.41 ± 5.98*

74.82 ± 6.04@

36.31 ± 1.29@

39.96 ± 1.91@

53.26 ± 1.93@

 % of change

↓5.92

↑7.54

↓34.01@

↓73.6@,†

↓74.76@,†

↓43.41@

4 weeks after treatment

83.50 ± 1.24

183.41 ± 4.37*

65.25 ± 1.67#

21.51 ± 0.83#

15.15 ± 0.77#

21.9  ± 0.77#

 % of change

↓10.32

↑2.99

↓42.53#,‡

↓84.28#,†

↓90.49#,†

↓76.79#

Data represent mean ± SE of each group, N = 8

* Significance at P < 0.01 for all groups versus normal control group

@Significance at P < 0.01 for all treated groups versus hypercholesterolaemic control group after 2 weeks of treatment

#Significance at P < 0.01 for all treated groups versus hypercholesterolaemic control group after 4 weeks of treatment

Significance at P < 0.01 for ginger groups (200 and 400 mg/kg) after 2 and 4 weeks of treatment versus atorvastatin

Significance at P < 0.01 for ginger group (100 mg/kg) after 2 and 4 weeks of treatment versus atorvastatin

Table 3

Effect of oral administration of aqueous ginger infusion (100, 200 and 400 mg/kg) and atorvastatin (0.18 mg/kg) in serum LDL-cholesterol level (mg/dL) after 2 and 4 weeks of treatment in hypercholesterolaemic rat model

Time

Normal control

Hypercholesterolaemic control

Ginger 100 mg/kg

Ginger 200 mg/kg

Ginger 400 mg/kg

Atorvastatin 0.18 mg/kg

Baseline before treatment

109.84 ± 1.59

307.13 ± 8.28*

177.32 ± 3.53*

189.32 ± 6.19*

209.6 ± 4.39*

176.29 ± 1.27*

2 weeks after treatment

108.24 ± 2.36

312.38 ± 13.79*

13.52 ± 1.31@

11.7 ± 1@

19.9 ± 1.12@

26.33 ± 0.67@

 % of change

↓1.36

↑2.05

↓92.31@,†

↓93.81@,†

↓90.42@,†

↓85.05@

4 weeks after treatment

112.21 ± 0.81

315.4 ± 9.15*

6.23 ± 0.44#

4.04 ± 0.24#

3.01 ± 0.35#

24.75 ± 0.96#

 % of change

↑2.27

↑2.81

↓96.48#,†

↓97.86#,†

↓98.56#,†

↓85.96#

Data represent mean ± SE of each group, N = 8

LDL-C low-density lipoprotein cholesterol

* Significance at P < 0.01 for all groups versus normal control group

@Significance at P < 0.01 for all treated groups versus hypercholesterolaemic control group after 2 weeks of treatment

#Significance at P < 0.01 for all groups versus hypercholesterolaemic control group after 4 weeks of treatment

Significance at P < 0.01 for all ginger groups (100, 200 and 400 mg/kg) after 2 and 4 weeks of treatment versus atorvastatin

Table 4

Effect of oral administration of aqueous ginger infusion (100, 200 and 400 mg/kg) and atorvastatin (0.18 mg/kg) in serum HDL-cholesterol level (mg/dL) after 2 and 4 weeks of treatment in hypercholesterolaemic rat model

Time

Normal control

Hypercholesterolaemic control

Ginger 100 mg/kg

Ginger 200 mg/kg

Ginger 400 mg/kg

Atorvastatin 0.18 mg/kg

Baseline before treatment

 HDL

49.49 ± 1.45

46.26 ± 1.8

45.62 ± 1.99

46.25 ± 0.92

41.62 ± 1.64

44.48 ± 0.9

 TC

180.79

385.86

244.75

263.97

283.12

240.66

 % HDL/TC

27.37

11.98*

18.63

17.52

14.7

18.48

2 weeks after treatment

 HDL

48.7 ± 1.36

59.39 ± 1.26*

75.14 ± 1.3

91.63 ± 1.39#

94.76 ± 1.96#

91.33 ± 0.91#

 TC

172.81

405.46

88.66

103.33

114.66

117.66

 % HDL/TC

28.18

14.64*

84.75#,†

88.67#,†

82.64#.†

77.62#

4 weeks after treatment

 HDL

50.67 ± 0.83

29.86 ± 0.93*

65.01 ± 1.05@

76.31 ± 1.59@

59.34 ± 1.11@

49.71 ± 0.75@

 TC

178.99

413.96

71.24

80.36

62.35

74.46

 % HDL/TC

28.3

7.21*

91.25@,†

94.96@,†

95.17@,†

66.76@

Data represent mean ± SE of each group, N = 8

HDL-C high-density lipoprotein cholesterol, TC total cholesterol

* Significance at P < 0.01 for serum HDL % to total serum cholesterol level of hypercholesterolaemic control group versus normal control group after 2 and 4 weeks of treatment

#Significance at P < 0.01 for all treated groups versus untreated hypercholesterolaemic control group after 2 weeks of treatment

@Significance at P < 0.01 for all treated groups versus hypercholesterolaemic control group after 4 weeks of treatment

Significance at P < 0.01 for all ginger groups versus atorvastatin group after 2 and 4 weeks of treatment

Table 5

Effect of oral administration of aqueous ginger infusion (100, 200 and 400 mg/kg) and atorvastatin (0.18 mg/kg) in risk ratio values (after 2 and 4 weeks of treatment in hypercholesterolaemic rat model

Time

Normal control

Hypercholesterolaemic control

Ginger 100 mg/kg

Ginger 200 mg/kg

Ginger 400 mg/kg

Atorvastatin 0.18 mg/kg

Baseline before treatment

3.57 ± 0.09

8.36 ± 0.28*

5.54 ± 0.24*

5.63 ± 0.15*

6.87 ± 0.34*

5.29 ± 0.04*

After 2 weeks of treatment

 Value

3.56 ± 0.09

6.83 ± 0.22

1.17 ± 0.06@

1.12 ± 0.03@

1.2 ± 0.05@

1.28 ± 0.05@

 % of change

↓0.18

↓17.85

↓78.88@

↓80.1@

↓82.53@,†

↓75.8@

After 4 weeks of treatment

 Value

3.53 ± 0.04

13.92 ± 0.4*

1.09 ± 0.03#

1.05 ± 0.03#

1.05 ± 0.03#

1.49 ± 0.11#

 % of change

↓0.51

↑68.26*

↓80.32#,†

↓81.34#,†

↓84.71#,†

↓71.83#

Data represent mean ± SE of each group, N = 8

* Significance at P < 0.01 for all groups versus normal control group

@Significance at P < 0.01 for all treated groups versus hypercholesterolaemic control group after 2 weeks of treatment

#Significance at P < 0.01 for all treated groups versus hypercholesterolaemic control group after 4 weeks of treatment

Significance at P < 0.01 for ginger group (400 mg/kg) after 2 weeks of treatment and all ginger groups after 4 weeks of treatment versus atorvastatin

Discussion

The present work was carried out to study the effect of aqueous ginger infusion (Z. officinale) as an antihypercholesterolaemic agent in adult albino rats (in vivo), where the dose of 200 mg/kg of ginger is equivalent in the efficacy to that of atorvastatin while the dose 400 mg/kg of ginger is more effective as hypocholesterolaemic agent than atorvastatin when given for the same duration of time under the same conditions of diet and life style for the treatment of the same pathologic condition. The [E]-8b,17-epoxylabd-12-ene-15,16-dial (ZT) compound that was isolated from ginger lowered plasma cholesterol levels in experimentally induced hypercholesterolaemia in rats by inhibiting cholesterol biosynthesis, and also interfered with cholesterol biosynthesis in homogenated liver of mice and rats (Tanabe et al. 1993). In rabbits fed high cholesterol diets, oral administration of ginger ethanol extracts had reduced atherogenesis and high lipid levels. In animal studies, ginger oleo-resin and dried ginger rhizome were found to reduce hypercholesterolaemia. The speculated mechanism for these compounds is by disrupting cholesterol absorption from the gastro-intestinal tract (Bhandari et al. 2005). The results in the present study may also be due to pharmacological action of ginger which elevates the activity of hepatic cholesterol 7α-hydroxylase that is a rate-limiting enzyme in the biosynthesis of bile acids and stimulating the conversion of cholesterol to bile acids thus leading to the excretion of cholesterol from the body (Srinivasan and Sambaiah 1991).

Moreover, the hypocholesterolaemic effects of ginger may be due to inhibition of cellular cholesterol synthesis (Ness et al. 1996). This may be due to the presence of niacin in ginger as reported in many studies that niacin causes increased clearance of VLDL, lowers triglyceride levels, increased hepatic uptake of LDL and inhibition of cholesterogenesis (Durrington 2003; Gardia 1990; Mary and John 2000). Aqueous infusion of ginger (5%) yielded nearly the same antioxidant activity toward lipid peroxidation as did the synthetic antioxidant butylhydroxyanisole (BHT) that is used to decelerate degradation of lipids. This result may be due to the essential oil content of the extract (Murcia et al. 2004). Also, the antioxidant activity of ginger stems from its high content of polyphones (Yen et al. 2003) and the antioxidant vitamin C (Benzie and Szeto 1999). Ginger powder significantly reduces the extent of lipid peroxidation and improves plasma antioxidant capacity. Augmentation of plasma antioxidant capacity decreases plasma-free radicals (Afshari et al. 2007). Moreover, polyphenolic flavonoids present in ginger may prevent coronary artery disease by reducing plasma cholesterol levels or by inhibiting LDL oxidation (Belinky et al. 1998). The main antioxidant active principles in ginger are the polyphenolic compounds gingerols, shogaols and some related phenolic ketone derivatives. Gingerol from ginger inhibited at high concentrations ascorbate/ferrous complex induced lipid peroxidation in rat liver microsomes (Reddy and Lokesh 1992). Ginger antioxidative effect may play an important role in attenuation development of atherosclerosis besides reducing plasma lipid levels in mice; the effect of ginger could be due to inhibiting and/or scavenging radicals of rat body in different degrees (Liu et al. 2003). When ginger was added to animal diet, a considerable increase in the pancreatic and intestine lipase occurred; lipase is the other key factor which plays a vital role in fat digestion (Platel and Srinivasan 2000). In the present work, reduction in serum triglycerides is dose dependent. Also, doses of 200 and 400 mg/kg of ginger are more effective as antihypercholesterolaemic than atorvastatin when given for 4 weeks and are equivalent to it when given for shorter period (2 weeks) under the same conditions of diet and life style for the treatment of the same pathologic condition. The triglycerides lowering effect of ginger may be due to ginger’s ability to enhance lipase activity (Bhandari et al. 1998). Increased clearance of VLDL via lipoprotein lipase pathway contributes to the triglycerides lowering effect of niacin (which as previously mentioned is a constituent of ginger). The clearance of triglyceride by lipoprotein lipase is saturated at about 800 mg/dL of triglyceride. In severe mixed lipemia, niacin often produces marked reduction in triglyceride levels in plasma; the LDL lowering effect is most probably because niacin (constituent of ginger) inhibits VLDL secretion, in turn decreases production of LDL. Attenuation of cholesterol synthesis results in augmentation of LDL receptor activity that leads to elimination of LDL from plasma (Ness et al. 1996). The increase in HDL is because niacin (a constituent of ginger) causes reduction in the catabolic rate of HDL (Mary and John 2000). One research reported that consumption of 500 mg of curcumin (a constituent of ginger) by volunteers for 10 days induced an increase in HDL-C by 29% (Soni et al. 1992).

Observed antihyperlipidemia effect of ginger may also be explained by the presence of high fiber and antinutrients such as phytic acid (Sharma 1980). In summary, results of the present work demonstrated that the use of aqueous ginger infusion at dose 100, 200 and 400 mg/kg has antihypercholesterolaemic effect which is more effective to more extent than a standard hypocholesterolaemic drug (atorvastatin) especially with high doses 200 and 400 mg/kg that were used. Based on these results, it is concluded that ginger in aqueous form may have therapeutic potential as antihypercholesterolaemic agent which is easily available to use and also it has a beneficial effect being more cheaper than other current hypolipidemic drugs. This may be a novel finding because the other previous studies were done with ethanol extract of ginger not with aqueous infusion and also used other animal models as rabbits or even in streptozotocin (STZ)-induced diabetes in rats not in normal rats. So, we can use aqueous ginger infusion as supplementation with current hypolipidemic drugs to reduce their doses and to overcome the possible side effect of these drugs.

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Copyright information

© Springer Basel AG 2010

Authors and Affiliations

  • El-Sayed M. ElRokh
    • 1
  • Nemat A. Z. Yassin
    • 2
  • Siham M. A. El-Shenawy
    • 2
  • Bassant M. M. Ibrahim
    • 2
  1. 1.Department of Pharmacology, Faculty of MedicineCairo UniversityCairoEgypt
  2. 2.Department of PharmacologyNational Research CentreCairoEgypt

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