Comparative Study of Anti-Cancer Properties of crude ethanolic ginger rhizome extract and Luteolin in EAC-Bearing Mice

Document Type : Original Article

Authors

1 Chemistry Department, Biochemistry Division, Faculty of Science, Mansoura University, 35516 Mansoura, Egypt.

2 Chemistry Department, Faculty of Science, Mansoura University

3 Genetic Unit, Children Hospital, Mansoura University, Egypt

4 Mansoura University, Faculty of Science

Abstract

Abstract

Nowadays, the use of plant medicine is a growing trend due to its decreased toxicity and potency. Moreover, several plants based bioactive compounds exert significant impact against various life-threatening diseases. In the light of the previous facts, we investigated the anti-cancer properties of Ginger (G) and Luteolin (LUT) in Ehrlich Ascites Carcinoma (EAC) bearing mice. 56 Swiss albino mice were used and divided into seven groups (8 per group) as follows: control group (C), control Ginger (G), control Luteolin (LUT), Ehrlich Ascites Carcinoma group (EAC), (EAC+G) group, (EAC+LUT) group, and (EAC+G+LUT) group. The (EAC), (EAC+G), (EAC+LUT) and (EAC+G+LUT) groups were intraperitoneally injected by Ehrlich cells 3x106 cells to induce Ehrlich tumor. The (G) and (LUT) groups were treated with ginger oral dose (200 mg/kg/day) and LUT (100 mg/ body weight/ day), respectively. Body weight was measured, and blood samples were taken for liver enzymes analysis. After that, the mice were sacrificed, and their liver tissues were obtained for histopathological investigation. Flow cytometry was utilized for cell cycle analysis, evaluation of Caspase-3, Ki67, and BCl-2. Also, Real-time PCR was used for VEGF expression. In this study, liver enzymes and histopathological examination were significantly improved upon treatment with Ginger and Luteolin. Moreover, the combined treatment of Ginger and Luteolin exhibited a potential antiproliferative activity against EAC more than single therapy, they exerted their effect by initiating apoptosis through regulating Caspase-3, Bcl-2, inhibit proliferation and arrest the cell cycle through inhibition of Ki-67.

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