Ginger extract (Zingiber officinale) has anti-cancer and anti-inflammatory effects on ethionine-induced hepatoma rats

Shafina Hanim Mohd Habib, Suzana Makpol, Noor Aini Abdul Hamid, Srijit Das, Wan Zurinah Wan Ngah, Yasmin Anum Mohd Yusof, Shafina Hanim Mohd Habib, Suzana Makpol, Noor Aini Abdul Hamid, Srijit Das, Wan Zurinah Wan Ngah, Yasmin Anum Mohd Yusof

Abstract

Objective: To evaluate the effect of ginger extract on the expression of NFkappaB and TNF-alpha in liver cancer-induced rats.

Methods: Male Wistar rats were randomly divided into 5 groups based on diet: i) control (given normal rat chow), ii) olive oil, iii) ginger extract (100mg/kg body weight), iv) choline-deficient diet + 0.1% ethionine to induce liver cancer and v) choline-deficient diet + ginger extract (100mg/kg body weight). Tissue samples obtained at eight weeks were fixed with formalin and embedded in paraffin wax, followed by immunohistochemistry staining for NFkappaB and TNF-alpha.

Results: The expression of NFkappaB was detected in the choline-deficient diet group, with 88.3 +/- 1.83% of samples showing positive staining, while in the choline-deficient diet supplemented with ginger group, the expression of NFkappaB was significantly reduced, to 32.35 +/- 1.34% (p<0.05). In the choline-deficient diet group, 83.3 +/- 4.52% of samples showed positive staining of TNF-alpha, which was significantly reduced to 7.94 +/- 1.32% (p<0.05) when treated with ginger. There was a significant correlation demonstrated between NFkappaB and TNF-alpha in the choline-deficient diet group but not in the choline-deficient diet treated with ginger extract group.

Conclusion: In conclusion, ginger extract significantly reduced the elevated expression of NFkappaB and TNF-alpha in rats with liver cancer. Ginger may act as an anti-cancer and anti-inflammatory agent by inactivating NFkappaB through the suppression of the pro-inflammatory TNF-alpha.

Figures

Figure 1
Figure 1
H & E staining on liver tissue of (A) control group (given a normal diet) (B) CDE group without treatment of CV (liver cancer was induced with 0.1% ethionine in drinking water plus a choline-deficient diet). H: Hepatocyte, K: Kuppfer cell, PV: Portal vein, S: Sinusoid, O: Oval cell (magnification ×400)
Figure 2
Figure 2
Immunohistochemical expression of NFkB. (A) Positive NFκB staining in cervical cancer tissue at optimum concentration of 1:500, (B) Control group (C) Ginger extract group, (D) Choline deficient diet with ethionine in drinking water, CDE group and (E) CDE + ginger extract (100 mg/kg body wt) group. The arrows indicate positive staining of NFkB (400x). OV: oval cells; H: hepatocytes; S: sinosoids; VP; vena portal (x400)
Figure 3
Figure 3
The effect of ginger extract on NFkB expression in liver cancer-induced rats. The graph shows the positive expression of NFkB based on the different diets given. A = p ≤ 0.05 compared with eight-week control group; b = p ≤ 0.05 compared with olive oil group; c = p ≤ 0.05 compared with ginger group; d = p ≤ 0.05 compared with liver cancer induced group (CDE); e = p ≤ 0.05 compared with CDE+ginger group
Figure 4
Figure 4
Immunohistochemical expression of TNF-α. (A) Positive control for TNF-α staining in breast cancer tissue at optimum concentration of 1:100; (B) Control group; (C) Ginger extract group; (D) CDE group; and (E) CDE + ginger extract group. The arrows indicate positive staining of TNF-α (400x). OV: oval cells; H: hepatocytes; S: sinosoids; VP; vena portal
Figure 5
Figure 5
The effect of ginger extract on TNF-α expression in rats with induced liver cancer. The graph shows the positive expression of TNF-α based on the different diets given. a = p ≤ 0.05 compared with eight-week control group; b = p ≤ 0.05 compared with olive oil group; c = p ≤ 0.05 compared with ginger group; d = p ≤ 0.05 compared with CDE group; e = p ≤ 0.05 compared with CDE+ginger group
Figure 6
Figure 6
Correlation coefficient between NFkB and TNF-α expressions in (A) CDE group and in (B) CDE supplemented with ginger extract (100 mg/kg body weight) group. Significant correlation was observed between NFkB and TNF-α in CDE group (r = 0.8776, p

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Source: PubMed

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