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Methyl palmitate reversed estradiol benzoate-induced endometrial hyperplasia in female rats.
Toxicol Mech Methods. 2021 Jan; 31(1):43-52.TM

Abstract

Early detection and treatment of endometrial hyperplasia (EH) is mandatory for endometrial cancer prevention. Several bioactive agents of plant origin have been shown to elicit their chemotherapeutic effect against tumors and cancer via induction of mitochondrial permeability transition(mPT) pore opening. This research was therefore aimed at evaluating the potential chemopreventive effect of methyl palmitate (MP), on estradiol benzoate(EB)-induced EH, looking at the mitochondrial-mediated pathway and other possible mechanisms of action. Mitochondria were isolated using differential centrifugation. The mPT pore, mitochondrial ATPase (mATPase) activity, lipid peroxidation and cytochrome c release were determined by standard methods using spectrophotometer. Uterine interleukin 1b, MDA levels and SOD, GSH activities, were determined using commercially available kits. The uterine histological and immunohistochemical assessment of estrogen receptor (ERα), IL-1b and caspas-3 were carried out. The fibroblast cell count density was determined using histomorphometry. At all the concentrations of MP used, there was no significant induction of mPT pore opening, neither any enhancement of mATPase activity nor release of cytochrome c when compared to the control. Similar pattern of results were recorded for the in vivo study. However, there was marked increase in the uterine MDA and interleukin 1b levels, with concurrent decrease in SOD and GSH activities, in the EB-treated group, which was significantly reversed by MP co-administration. Endometrial Hyperplasia observed in the EB-treated group was ameliorated by MP co-administration. The immunoexpression of ERα and IL-1b in the EB-treated group was reversed by MP co-administration. This study suggests anti-inflammatory, antioxidant and anti-proliferative potential of MP against EB-induced EH.

Authors+Show Affiliations

Laboratory for Membrane Biochemistry Research and Biotechnology, Department of Biochemistry, Faculty of Basic Medical Sciences, College of Medicine, University of Ibadan, Ibadan, Nigeria.Laboratory for Membrane Biochemistry Research and Biotechnology, Department of Biochemistry, Faculty of Basic Medical Sciences, College of Medicine, University of Ibadan, Ibadan, Nigeria.Laboratory for Membrane Biochemistry Research and Biotechnology, Department of Biochemistry, Faculty of Basic Medical Sciences, College of Medicine, University of Ibadan, Ibadan, Nigeria.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32967526

Citation

Olowofolahan, Adeola O., et al. "Methyl Palmitate Reversed Estradiol Benzoate-induced Endometrial Hyperplasia in Female Rats." Toxicology Mechanisms and Methods, vol. 31, no. 1, 2021, pp. 43-52.
Olowofolahan AO, Oyebode OT, Olorunsogo OO. Methyl palmitate reversed estradiol benzoate-induced endometrial hyperplasia in female rats. Toxicol Mech Methods. 2021;31(1):43-52.
Olowofolahan, A. O., Oyebode, O. T., & Olorunsogo, O. O. (2021). Methyl palmitate reversed estradiol benzoate-induced endometrial hyperplasia in female rats. Toxicology Mechanisms and Methods, 31(1), 43-52. https://doi.org/10.1080/15376516.2020.1827329
Olowofolahan AO, Oyebode OT, Olorunsogo OO. Methyl Palmitate Reversed Estradiol Benzoate-induced Endometrial Hyperplasia in Female Rats. Toxicol Mech Methods. 2021;31(1):43-52. PubMed PMID: 32967526.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Methyl palmitate reversed estradiol benzoate-induced endometrial hyperplasia in female rats. AU - Olowofolahan,Adeola O, AU - Oyebode,Olubukola T, AU - Olorunsogo,Olufunso O, Y1 - 2020/10/06/ PY - 2020/9/25/pubmed PY - 2021/4/1/medline PY - 2020/9/24/entrez KW - Methyl palmitate KW - apoptosis KW - endometrial hyperplasia KW - estradiol benzoate KW - mitochondrial permeability transition pore SP - 43 EP - 52 JF - Toxicology mechanisms and methods JO - Toxicol Mech Methods VL - 31 IS - 1 N2 - Early detection and treatment of endometrial hyperplasia (EH) is mandatory for endometrial cancer prevention. Several bioactive agents of plant origin have been shown to elicit their chemotherapeutic effect against tumors and cancer via induction of mitochondrial permeability transition(mPT) pore opening. This research was therefore aimed at evaluating the potential chemopreventive effect of methyl palmitate (MP), on estradiol benzoate(EB)-induced EH, looking at the mitochondrial-mediated pathway and other possible mechanisms of action. Mitochondria were isolated using differential centrifugation. The mPT pore, mitochondrial ATPase (mATPase) activity, lipid peroxidation and cytochrome c release were determined by standard methods using spectrophotometer. Uterine interleukin 1b, MDA levels and SOD, GSH activities, were determined using commercially available kits. The uterine histological and immunohistochemical assessment of estrogen receptor (ERα), IL-1b and caspas-3 were carried out. The fibroblast cell count density was determined using histomorphometry. At all the concentrations of MP used, there was no significant induction of mPT pore opening, neither any enhancement of mATPase activity nor release of cytochrome c when compared to the control. Similar pattern of results were recorded for the in vivo study. However, there was marked increase in the uterine MDA and interleukin 1b levels, with concurrent decrease in SOD and GSH activities, in the EB-treated group, which was significantly reversed by MP co-administration. Endometrial Hyperplasia observed in the EB-treated group was ameliorated by MP co-administration. The immunoexpression of ERα and IL-1b in the EB-treated group was reversed by MP co-administration. This study suggests anti-inflammatory, antioxidant and anti-proliferative potential of MP against EB-induced EH. SN - 1537-6524 UR - https://www.unboundmedicine.com/medline/citation/32967526/Methyl_palmitate_reversed_estradiol_benzoate_induced_endometrial_hyperplasia_in_female_rats_ L2 - https://www.tandfonline.com/doi/full/10.1080/15376516.2020.1827329 DB - PRIME DP - Unbound Medicine ER -