Methyl palmitate reversed estradiol benzoate-induced endometrial hyperplasia in female rats

Olowofolahan, Adeola Oluwakemi; Oyebode, Olubukola T.; Olorunsogo, Olufunso O.

doi:10.1080/15376516.2020.1827329

Cited by 13 publications

(13 citation statements)

References 34 publications

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“…Estrogen metabolites produce reactive oxygen species capable of inducing peroxidative damage to cellular membranes [ 28 ]. In agreement with the present study, previous reports [ 29 , 30 ] showed similar findings relating to the ability of EB to increase the lipid peroxidation product MDA, a known marker of oxidative stress, in EB-induced EH in female rats. Similarly, EB can increase oxidative stress in EH by decreasing the endogenous antioxidant enzyme SOD [ 29 , 30 ].…”

Section: Discussionsupporting

confidence: 94%

“…In agreement with the present study, previous reports [ 29 , 30 ] showed similar findings relating to the ability of EB to increase the lipid peroxidation product MDA, a known marker of oxidative stress, in EB-induced EH in female rats. Similarly, EB can increase oxidative stress in EH by decreasing the endogenous antioxidant enzyme SOD [ 29 , 30 ]. SOD effectively shields from oxidative stress by dismutation of superoxide radicals to hydrogen peroxide [ 31 ].…”

Section: Discussionsupporting

confidence: 94%

“…Finally, compatible with previous reports [29,30], the current study showed the characteristic histopathological changes of EB-induced EH and atypia. On the other hand, IRB was able to prevent the damage produced by EB administration, thus providing further support to the suggestive mechanism of action of IRB.…”

Section: Discussionsupporting

confidence: 93%

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Protective Effects of Irbesartan, an Angiotensin Receptor Blocker with PPARγ Agonistic Activity, against Estradiol Benzoate-Induced Endometrial Hyperplasia and Atypia in Female Rats via Modulation of TNFα/Survivin Pathway

et al. 2021

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Endometrial hyperplasia (EH) is a common gynecological problem and may progress to carcinoma. Early detection and management of EH are mandatory for the prevention of endometrial cancer. Activation of the renin–angiotensin system and angiotensin II signaling are involved in the progression of precancerous and cancerous lesions. However, no studies have evaluated the role of this system in estradiol benzoate (EB)-induced EH and atypia. Irbesartan (IRB), an angiotensin II receptor blocker with peroxisome proliferator-activated receptor gamma (PPARγ) agonistic activity was administered (30 mg/kg/d) in EB-treated (60 µg/100 g bodyweight, intramuscularly, three times per week) or untreated rats for 4 weeks. Uterine weight changes, malondialdehyde, superoxide dismutase (SOD), tumor necrosis factor-alpha (TNFα), survivin, cleaved caspase 3, interleukin-10 (IL10), and PPARγ were measured in addition to undergoing histopathological examination. Results showed that EB-induced EH and atypia significantly increased the uterine body weight, malondialdehyde, TNFα, and survivin, accompanied with significantly decreased SOD, cleaved caspase 3, IL10, and PPARγ, with typical histopathological changes of EH and atypia. Coadministration of IRB significantly prevented EB-induced biochemical and histopathological changes. The protective effects of IRB may be attributed to its anti-inflammatory and antioxidant properties, reduction of survivin, and increased levels of cleaved caspase 3.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 94%

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Protective Effects of Irbesartan, an Angiotensin Receptor Blocker with PPARγ Agonistic Activity, against Estradiol Benzoate-Induced Endometrial Hyperplasia and Atypia in Female Rats via Modulation of TNFα/Survivin Pathway

et al. 2021

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“…It has been reported that unopposed high estrogen treatment can cause increase in reactive oxygen species (ROS) resulting to DNA, protein and lipid damage (Gupta et al 2015;Pescatori et al 2021). The elevated MDA level in the EB-treated rats could be attributed to EB-induced oxidative stress (Olowofolahan et al 2020;Pejic et al 2009). This was reversed by metformin coadministration.…”

Section: Discussionmentioning

confidence: 99%

“…Different doses of metformin (MTF) were orally administered while EB was intraperitoneally administered. The chosen doses were based on pilot study and literature search (Jing et al 2019;Diniz Vilela et al 2016;Olowofolahan et al 2020).…”

Section: Chemicals and Reagentsmentioning

confidence: 99%

Metformin induces apoptosis via uterus mitochondrial permeability transition pore opening and protects against estradiol benzoate-induced uterine defect and associated pathophysiological disorder in female Wistar rats

2021

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Background Some antitumor or anticancer agents have been shown to execute cell death by induction of mitochondrial permeability transition (mPT) pore opening in order to elicit their chemotherapeutic effect. Therefore, this study investigated the effect of metformin on cell death via rat uterus mPT pore and estradiol benzoate-induced uterine defect and associated pathophysiological disorder in female rat. Mitochondria were isolated using differential centrifugation. The mPT pore opening, cytochrome c release and mitochondrial ATPase activity were determined spectrophotometrically. Caspases 9 and 3 activities, MDA and estradiol levels and SOD, GSH activities, were determined using ELISA technique. Histological and histochemical assessments of the uterine section were carried out using standard methods. Results Metformin at concentrations 10–90 μg/mL, showed no significant effect on mPT pore opening, mATPase activity and release of cytochrome c. However, oral administration of metformin caused mPT pore opening, enhancement of mATPase activity and activation of caspases 9 and 3 significantly at 300 and 400 mg/kg. Metformin protected against estradiol benzoate (EB)-induced uterine defect and other associated pathophysiological disorder. It also improved the antioxidant defense system. The histological evaluation revealed the protective effect of metformin on the cellular architecture of the uterus while the histochemical examination showed severe hyperplasia in the uterine section of EB-treated rats, remarkably reversed by metformin co-treatment. Conclusion This study suggests that metformin at high doses induces apoptosis via rat uterus mPT pore opening and protects against EB-induced uterine defect (hyperplasia) and associated pathophysiological disorder.

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Oleic acid induces mitochondrial-mediated cell death via mPT pore and protects against estradiol benzoate-induced endometrial hyperplasia in female Wistar rats

Olowofolahan,

Aina,

Olorunsogo

2024

Comp Clin Pathol

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Methyl palmitate reversed estradiol benzoate-induced endometrial hyperplasia in female rats

Cited by 13 publications

References 34 publications

Protective Effects of Irbesartan, an Angiotensin Receptor Blocker with PPARγ Agonistic Activity, against Estradiol Benzoate-Induced Endometrial Hyperplasia and Atypia in Female Rats via Modulation of TNFα/Survivin Pathway

Protective Effects of Irbesartan, an Angiotensin Receptor Blocker with PPARγ Agonistic Activity, against Estradiol Benzoate-Induced Endometrial Hyperplasia and Atypia in Female Rats via Modulation of TNFα/Survivin Pathway

Metformin induces apoptosis via uterus mitochondrial permeability transition pore opening and protects against estradiol benzoate-induced uterine defect and associated pathophysiological disorder in female Wistar rats

Oleic acid induces mitochondrial-mediated cell death via mPT pore and protects against estradiol benzoate-induced endometrial hyperplasia in female Wistar rats

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