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

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dc.contributor.authorMichael OS
dc.contributor.authorDibia CL
dc.contributor.authorAdeyanju OA
dc.contributor.authorOlaniyi KS
dc.contributor.authorAreola ED
dc.contributor.authorOlatunji LA
dc.date.accessioned2022-07-28T19:33:05Z
dc.date.available2022-07-28T19:33:05Z
dc.date.issued2020
dc.descriptionBiomedicine & Pharmacotherapy
dc.description.abstractApproximately 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.
dc.identifier.citation10.1016/j.biopha.2020.110387
dc.identifier.issn0753-3322
dc.identifier.urihttps://nerd.ethesis.ng/handle/123456789/460
dc.language.isoen
dc.subjectEstrogen-progestin therapy
dc.subjectCardiac Na-K-ATPase activity
dc.subjectLipid
dc.subjectInsulin resistance
dc.subjectMetabolic stress
dc.subjectNicotine
dc.titleEstrogen-progestin oral contraceptive and nicotine exposure synergistically confers cardio-renoprotection in female Wistar rats
dc.typeArticle
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