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Cimetidine a promising radio-protective agent through modulating Bax/Bcl2 ratio: An in vivo study in male rats.
J Cell Physiol. 2020 Apr 23 [Online ahead of print]JC

Abstract

Radiotherapy is one of the most effective modalities for treatment of neoplastic diseases. Radiation damage is to a large extent caused by overproduction of reactive oxygen species. To improve the therapeutic index, identifying effective substances for prevention or treatment of postirradiation intestinal and bone marrow injury should be prompted. This study was designed to evaluate the protective effects of cimetidine on the in rats exposed to γ-irradiation (5 Gy) and exploring the B-cell lymphoma 2 (Bcl2)/Bcl2 associated X (bax) pathway as a probable underlying mechanism. Eighteen adult male rats were randomly grouped into three: control, untreated irradiated rats, and irradiated rats pretreated with cimetidine. Seven days postirradiation the rats were culled, the bone marrow (BM) and jejunum tissue samples were collected for biochemical, histological, and immunohistological evaluation of BM cell count (BMCs), intestinal fibrosis, oxidative stress, tumor necrosis factor-α, Bcl2, and Bax. Cimetidine pretreatment significantly reversed the loss of BMCs, intestinal lining destruction, and fibrosis seen in the untreated irradiated rats and significantly decreased the underlying oxidative stress, inflammation, and Bax/Bcl2 ratio. There was a significant differential correlation between Bax/Bcl2 ratio, tissue oxidative stress level, and tissue injury. Cimetidine represents a very promising radioprotective agent with a potential differential beneficial effect on both cancer cells (inducing apoptosis) as previously proved through different studies and adjacent healthy cells (providing radioprotection via inhibiting apoptosis) as clearly demonstrated through this study, via its antioxidant effect and subsequent regulation of type 2 apoptotic pathway through modulation of Bax/Bcl2 ratio.

Authors+Show Affiliations

Physiology Department, Faculty of Medicine, Cairo University, Cairo, Egypt. ANU Medical School, Australian National University, Canberra, ACT, Australia.Clinical Oncology, Faculty of Medicine, Cairo University, Cairo, Egypt.Biochemistry Department, Faculty of Medicine, Cairo University, Cairo, Egypt.Department of Anatomy, College of Medicine, Qassim University, Meleda, KSA. Anatomy Department, Faculty of Medicine, Cairo University, Cairo, Egypt.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32324265

Citation

Estaphan, Suzanne, et al. "Cimetidine a Promising Radio-protective Agent Through Modulating Bax/Bcl2 Ratio: an in Vivo Study in Male Rats." Journal of Cellular Physiology, 2020.
Estaphan S, Abdel-Malek R, Rashed L, et al. Cimetidine a promising radio-protective agent through modulating Bax/Bcl2 ratio: An in vivo study in male rats. J Cell Physiol. 2020.
Estaphan, S., Abdel-Malek, R., Rashed, L., & Mohamed, E. A. (2020). Cimetidine a promising radio-protective agent through modulating Bax/Bcl2 ratio: An in vivo study in male rats. Journal of Cellular Physiology. https://doi.org/10.1002/jcp.29692
Estaphan S, et al. Cimetidine a Promising Radio-protective Agent Through Modulating Bax/Bcl2 Ratio: an in Vivo Study in Male Rats. J Cell Physiol. 2020 Apr 23; PubMed PMID: 32324265.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cimetidine a promising radio-protective agent through modulating Bax/Bcl2 ratio: An in vivo study in male rats. AU - Estaphan,Suzanne, AU - Abdel-Malek,Raafat, AU - Rashed,Laila, AU - Mohamed,Enas Ahmed, Y1 - 2020/04/23/ PY - 2019/09/05/received PY - 2020/02/17/revised PY - 2020/03/22/accepted PY - 2020/4/24/entrez KW - Bax KW - Bcl2 KW - TNF-α KW - cimetidine KW - ionizing radiation KW - oxidative stress JF - Journal of cellular physiology JO - J. Cell. Physiol. N2 - Radiotherapy is one of the most effective modalities for treatment of neoplastic diseases. Radiation damage is to a large extent caused by overproduction of reactive oxygen species. To improve the therapeutic index, identifying effective substances for prevention or treatment of postirradiation intestinal and bone marrow injury should be prompted. This study was designed to evaluate the protective effects of cimetidine on the in rats exposed to γ-irradiation (5 Gy) and exploring the B-cell lymphoma 2 (Bcl2)/Bcl2 associated X (bax) pathway as a probable underlying mechanism. Eighteen adult male rats were randomly grouped into three: control, untreated irradiated rats, and irradiated rats pretreated with cimetidine. Seven days postirradiation the rats were culled, the bone marrow (BM) and jejunum tissue samples were collected for biochemical, histological, and immunohistological evaluation of BM cell count (BMCs), intestinal fibrosis, oxidative stress, tumor necrosis factor-α, Bcl2, and Bax. Cimetidine pretreatment significantly reversed the loss of BMCs, intestinal lining destruction, and fibrosis seen in the untreated irradiated rats and significantly decreased the underlying oxidative stress, inflammation, and Bax/Bcl2 ratio. There was a significant differential correlation between Bax/Bcl2 ratio, tissue oxidative stress level, and tissue injury. Cimetidine represents a very promising radioprotective agent with a potential differential beneficial effect on both cancer cells (inducing apoptosis) as previously proved through different studies and adjacent healthy cells (providing radioprotection via inhibiting apoptosis) as clearly demonstrated through this study, via its antioxidant effect and subsequent regulation of type 2 apoptotic pathway through modulation of Bax/Bcl2 ratio. SN - 1097-4652 UR - https://www.unboundmedicine.com/medline/citation/32324265/Cimetidine_a_promising_radio-protective_agent_through_modulating_Bax/Bcl2_ratio:_An_in_vivo_study_in_male_rats L2 - https://doi.org/10.1002/jcp.29692 DB - PRIME DP - Unbound Medicine ER -
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