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Phikud Navakot Modulates the Level of Pro-Inflammatory Mediators and the Protein Expression of SOD1 and 2 and the Nrf2/HO-1 Signaling Pathway in Rats with Acute Myocardial Infarction

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dc.contributor.authorGerdprasert O.
dc.contributor.authorChoomchuay N.
dc.contributor.authorChantong B.
dc.contributor.authorSutanthavibul N.
dc.contributor.authorMeksuriyen D.
dc.contributor.authorNusuetrong P.
dc.date.accessioned2021-04-05T03:04:23Z
dc.date.available2021-04-05T03:04:23Z
dc.date.issued2019
dc.date.issuedBE2562
dc.description.abstractPhikud Navakot (PN) is nine major herbs in a famous traditional Thai recipe namely "Yahom Navakot" used to treat cardiovascular disorders. This study investigated the cardioprotective effects of PN formula on isoproterenol-induced myocardial infarction (IMI) in Sprague-Dawley rats. Forty-five rats were randomly divided into nine groups (n = 5 per group): the control, the IMI, the IMI + propranolol, the control or the IMI + PN formula (PN ethanolic extract at doses of 64, 127, or 255 mg/kg) by oroesophageal gavage for 28 days. The ST segment and serum troponin T levels were significantly increased in IMI rats. PN did not eliminate tissue necrosis, infiltration of inflammatory cells, or interstitial edema in IMI rats. All doses of PN decreased (p<0.001) serum TNF-α and IL-6 levels. PN (127 and 255 mg/kg) up-regulated (p<0.05) heme oxygenase (HO)-1 expression, whereas PN (255 mg/kg) significantly increased superoxide dismutase (SOD) 1 and 2 expression, compared with IMI rats. Nuclear factor erythroid 2-related factor 2 (Nrf2) and HO-1 expression significantly increased in IMI rats and IMI rats that received PN. PN formula possesses potential anti-inflammatory and antioxidant properties by modulating the levels of TNF-α, IL-6 and antioxidant enzymes. Our study reveals a novel cardioprotective effect of PN in IMI rats through the Nrf2/HO-1 signaling. © 2019 Orapin Gerdprasert et al.
dc.format.mimetypeapplication/pdf
dc.identifier.citationEvidence-based Complementary and Alternative Medicine. Vol 2019, (2019)
dc.identifier.doi10.1155/2019/4823645
dc.identifier.issn1741427X
dc.identifier.other2-s2.0-85073078632
dc.identifier.urihttps://hdl.handle.net/20.500.14740/5620
dc.rights.holderมหาวิทยาลัยศรีนครินทรวิโรฒ
dc.subject.otherAlcohol
dc.subject.otherAntiinflammatory agent
dc.subject.otherAntioxidant
dc.subject.otherCardiovascular agent
dc.subject.otherCatalase
dc.subject.otherCopper zinc superoxide dismutase
dc.subject.otherGlutathione peroxidase
dc.subject.otherHeme oxygenase 1
dc.subject.otherHerbaceous agent
dc.subject.otherInterleukin 6
dc.subject.otherManganese superoxide dismutase
dc.subject.otherPhikud navakot
dc.subject.otherPropranolol
dc.subject.otherProtective agent
dc.subject.otherTranscription factor Nrf2
dc.subject.otherTroponin T
dc.subject.otherTumor necrosis factor
dc.subject.otherUnclassified drug
dc.subject.otherAcute heart infarction
dc.subject.otherAnimal experiment
dc.subject.otherAnimal model
dc.subject.otherAnimal tissue
dc.subject.otherAntiinflammatory activity
dc.subject.otherAntioxidant activity
dc.subject.otherArticle
dc.subject.otherCell infiltration
dc.subject.otherControlled study
dc.subject.otherCytokine release
dc.subject.otherDrug dose comparison
dc.subject.otherDrug efficacy
dc.subject.otherDrug mechanism
dc.subject.otherEdema
dc.subject.otherEnzyme activity
dc.subject.otherEthnopharmacology
dc.subject.otherHeart muscle injury
dc.subject.otherHeart muscle necrosis
dc.subject.otherHeart protection
dc.subject.otherHeart tissue
dc.subject.otherInflammation
dc.subject.otherInflammatory cell
dc.subject.otherInflammatory infiltrate
dc.subject.otherInterstitial edema
dc.subject.otherIsoproterenol-induced myocardial infarction
dc.subject.otherMale
dc.subject.otherMediator release
dc.subject.otherNonhuman
dc.subject.otherOxidative stress
dc.subject.otherProtein blood level
dc.subject.otherProtein expression
dc.subject.otherRat
dc.subject.otherSignal transduction
dc.subject.otherST segment
dc.subject.otherTissue necrosis
dc.subject.otherUpregulation
dc.titlePhikud Navakot Modulates the Level of Pro-Inflammatory Mediators and the Protein Expression of SOD1 and 2 and the Nrf2/HO-1 Signaling Pathway in Rats with Acute Myocardial Infarction
dc.typeArticle
dspace.entity.typePublication
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