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. 2022 Jul 21:2022:9506026.
doi: 10.1155/2022/9506026. eCollection 2022.

In Vitro and In Vivo Antioxidant and Anticancer Potentials of Royal Jelly for Dimethylhydrazine-Induced Colorectal Cancer in Wistar Rats

Maede Shakib Khoob  1 , Seyed Mohammad Hosseini  1 , Sohrab Kazemi  2
Affiliations

In Vitro and In Vivo Antioxidant and Anticancer Potentials of Royal Jelly for Dimethylhydrazine-Induced Colorectal Cancer in Wistar Rats

Maede Shakib Khoob et al. Oxid Med Cell Longev. .

Abstract

Methods: This study was conducted among 60 rats, and groups consist of control, three separate groups for RJ, dimethylhydrazine (DMH), and vitamin E, and two separate treated groups with DMH + RJ and DMH + vitamin E. Additionally, the cytotoxicity of royal jelly was examined on HT-29 cell line. Findings. Based on the in vitro assessment using MTT assay, the LC50 of royal jelly was 1.781 mg/ml, and the highest cytotoxicity was observed at 25 mg/ml concentration after 48 hours. Meanwhile, in the in vivo study, after the 13th week, compared to the DMH group, the rats exposed to DMH + royal jelly experienced a significant less oxidative stress (P < 0.05) and a significantly greater total antioxidant capacity (TAC) level (P < 0.05). The expression of proliferating cell nuclear antigen (PCNA), platelet-derived growth factor (PDGF), and carcinoembryonic antigen (CEA) proteins significantly decreased among the animals receiving DMH + royal jelly compared to the DMH group. The pathological examinations revealed less congestion, necrosis, inflammation, and cell proliferation in the colon tissue of the RJ-treated group than that of the DMH group. Overall, the biochemical indices were better in the treatment groups in comparison with the DMH group.

Conclusion: The results represented the clinical usability of royal jelly, as a substance with anticancer properties, to prevent and treat colorectal cancer. This issue is related to its effective antioxidant potential, which even exhibits more effectiveness than the vitamin E, which is known as a strong antioxidant.

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Conflict of interest statement

The authors have no conflicts of interest to declare. All coauthors have seen and agree with the contents of the manuscript, and there is no financial interest to report. We certify that the submission is original work and is not under review at any other publication.

Figures

Figure 1
Figure 1
Viability level of HT-29 cells, as well as LC50. The results were read after 48 hours.
Figure 2
Figure 2
Comparison between the effects of royal jelly with various concentrations on cancer cells viability. Results are expressed as the mean ± standard error in mg/ml.
Figure 3
Figure 3
Comparison between general serum biochemical indices. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001: significant compared to the DMH group. All results are expressed as the mean ± standard error. n = 5.
Figure 4
Figure 4
MDA, SOD, and TAC levels in the different groups. ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001: significant compared to the DMH group. All results are expressed as the mean ± standard error. n = 5.
Figure 5
Figure 5
Comparison of colon tissues indices of the different groups. Normal tissue conditions in the control, royal jelly, and vitamin E groups. Mitosis, necrosis, and inflammatory cells which are illustrated with upward arrows, right arrows, and ∗, respectively, which can be seen in the DMH and treatment groups. ×40 magnification, H&E staining.
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References

    1. Lei L., Zhang J., Decker E. A., Zhang G. Roles of lipid peroxidation-derived electrophiles in pathogenesis of colonic inflammation and colon cancer. Frontiers in Cell and Developmental Biology . 2021;9 doi: 10.3389/fcell.2021.665591. - DOI - PMC - PubMed
    1. Guéraud F. 4-Hydroxynonenal metabolites and adducts in pre-carcinogenic conditions and cancer. Free Radical Biology and Medicine . 2017;111:196–208. doi: 10.1016/j.freeradbiomed.2016.12.025. - DOI - PubMed
    1. Grivennikov S. I. Inflammation and colorectal cancer: colitis-associated neoplasia. Seminars in Immunopathology . 2013;35(2):229–244. doi: 10.1007/s00281-012-0352-6. - DOI - PMC - PubMed
    1. Sharma S. H., Thulasingam S., Chellappan D. R., Chinnaswamy P., Nagarajan S. Morin and Esculetin supplementation modulates c-myc induced energy metabolism and attenuates neoplastic changes in rats challenged with the procarcinogen 1,2 - dimethylhydrazine. European Journal of Pharmacology . 2017;796:20–31. doi: 10.1016/j.ejphar.2016.12.019. - DOI - PubMed
    1. Glauert H. P., Bennink M. R. Metabolism of 1, 2-Dimethylhydrazine by Cultured Rat Colon Epithelial Cells. Nutrition and Cancer . 1983;5(2):78–86. doi: 10.1080/01635588309513782. - DOI - PubMed

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