Estrogen-progestin oral contraceptive and nicotine exposure synergistically confers cardio-renoprotection in female Wistar rats

Autor: Olugbenga Samuel Michael, Oluwaseun A. Adeyanju, Chinaza Dibia, Lawrence A. Olatunji, Kehinde S. Olaniyi, Emmanuel D. Areola
Jazyk: angličtina
Rok vydání: 2020
Předmět:
0301 basic medicine
Ethinyl Estradiol
Kidney
Nicotine
chemistry.chemical_compound
0302 clinical medicine
Hyperinsulinemia
Levonorgestrel
Nicotinic Agonists
Metabolic stress
Drug Synergism
Heart
General Medicine
Lipid
Malondialdehyde
Contraceptives
Oral
Combined
Drug Combinations
medicine.anatomical_structure
Estrogen-progestin therapy
030220 oncology & carcinogenesis
Female
Inflammation Mediators
Sodium-Potassium-Exchanging ATPase
hormones
hormone substitutes
and hormone antagonists
medicine.drug
medicine.medical_specialty
medicine.drug_class
RM1-950
Cardiac Na+-K+-ATPase activity
03 medical and health sciences
Internal medicine
medicine
Animals
Rats
Wistar
Pharmacology
business.industry
Myocardium
Estrogens
Insulin resistance
Nicotine replacement therapy
medicine.disease
Lipid Metabolism
Oxidative Stress
030104 developmental biology
Endocrinology
chemistry
Estrogen
Cytoprotection
Therapeutics. Pharmacology
Progestins
Cotinine
business
Zdroj: Biomedicine & Pharmacotherapy, Vol 129, Iss, Pp 110387-(2020)
ISSN: 0753-3322
Popis: Approximately fifty percent of premenopausal women who smoke cigarettes or on nicotine replacement therapy are also on hormonal contraceptives, especially oral estrogen-progestin. Oral estrogen-progestin therapy has been reported to promote insulin resistance (IR) which causes lipid influx into non-adipose tissue and impairs Na+/K+ -ATPase activity, especially in the heart and kidney. However, the effects of nicotine on excess lipid and altered Na+/K+ -ATPase activity associated with the use of estrogen-progestin therapy have not been fully elucidated. This study therefore aimed at investigating the effect of nicotine on cardiac and renal lipid influx and Na+/K+ -ATPase activity during estrogen-progestin therapy. Twenty-four female Wistar rats grouped into 4 (n = 6/group) received (p.o.) vehicle, nicotine (1.0 mg/kg) with or without estrogen-progestin steroids (1.0 μg ethinyl estradiol and 5.0 μg levonorgestrel) and estrogen-progestin only daily for 6 weeks. Data showed that estrogen-progestin treatment or nicotine exposure caused IR, hyperinsulinemia, increased cardiac and renal uric acid, malondialdehyde, triglyceride, glycogen synthase kinase-3, plasminogen activator inhibitor-1, reduced bilirubin and circulating estradiol. Estrogen-progestin treatment led to decreased cardiac Na+/K+-ATPase activity while nicotine did not alter Na+/K+-ATPase activity but increased plasma and tissue cotinine. Renal Na+/K+-ATPase activity was not altered by the treatments. However, all these alterations were reversed following combined administration of oral estrogen-progestin therapy and nicotine. The present study therefore demonstrates that oral estrogen-progestin therapy and nicotine exposure synergistically prevents IR-linked cardio-renotoxicity with corresponding improvement in cardiac and renal lipid accumulation, oxidative stress, inflammation and Na+/K+-ATPase activity.
Databáze: OpenAIRE
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