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Boldine improves kidney damage in the goldblatt 2K1C model avoiding the increase in TGF-β

dc.contributor.authorGómez G.I.
dc.contributor.authorVelarde V.
dc.date.accessioned2020-09-02T22:19:53Z
dc.date.available2020-09-02T22:19:53Z
dc.date.issued2018
dc.identifier10.3390/ijms19071864
dc.identifier.citation19, 7, -
dc.identifier.issn16616596
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4794
dc.descriptionBoldine, a major aporphine alkaloid found in the Chilean boldo tree, is a potent antioxidant. Oxidative stress plays a detrimental role in the pathogenesis of kidney damage in renovascular hypertension (RVH). The activation of the renin-angiotensin system (RAS) is crucial to the development and progression of hypertensive renal damage and TGF-β is closely associated with the activation of RAS. In the present study, we assessed the effect of boldine on the progression of kidney disease using the 2K1C hypertension model and identifying mediators in the RAS, such as TGF-β, that could be modulated by this alkaloid. Toward this hypothesis, rats (n = 5/group) were treated with boldine (50 mg/kg/day, gavage) for six weeks after 2K1C surgery (pressure ≥ 180 mmHg). Kidney function was evaluated by measuring of proteinuria/creatininuria ratio (U prot/U Crea), oxidative stress (OS) by measuring thiobarbituric acid reactive substances (TBARS). The evolution of systolic blood pressure (SBP) was followed weekly. Alpha-smooth muscle actin (α-SMA) and Col III were used as markers of kidney damage; ED-1 and osteopontin (OPN) were used as markers of inflammation. We also explored the effect in RAS mediators, such as ACE-1 and TGF-β. Boldine treatment reduced the UProt/UCrea ratio, plasma TBARS, and slightly reduced SBP in 2K1C hypertensive rats, producing no effect in control animals. In 2K1C rats treated with boldine the levels of α-SMA, Col III, ED-1, and OPN were lower when compared to 2K1C rats. Boldine prevented the increase in ACE-1 and TGF-β in 2K1C rats, suggesting that boldine reduces kidney damage. These results suggest that boldine could potentially be used as a nutraceutic. © 2018 by the authors. Licensee MDPI, Basel, Switzerland.
dc.language.isoen
dc.publisherMDPI AG
dc.subject(S)-2,9-dihydroxy-1,10-dimethoxy-aporphine
dc.subjectChronic kidney disease
dc.subjectFibrosis
dc.subjectOxidative stress
dc.subjectRenovascular hypertension
dc.subjectAbD Serotec
dc.subjectalpha smooth muscle actin
dc.subjectboldine
dc.subjectcollagen type 3
dc.subjectcreatinine
dc.subjectdipeptidyl carboxypeptidase
dc.subjectmonoclonal antibody
dc.subjectosteopontin
dc.subjectpotassium
dc.subjectreactive oxygen metabolite
dc.subjectsodium
dc.subjectthiobarbituric acid reactive substance
dc.subjecttransforming growth factor beta
dc.subjectaporphine derivative
dc.subjectboldine
dc.subjecttransforming growth factor beta
dc.subjectadult
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectantioxidant activity
dc.subjectArticle
dc.subjectcontrolled study
dc.subjectcreatinine clearance
dc.subjectdrug efficacy
dc.subjectdrug mechanism
dc.subjectenzyme linked immunosorbent assay
dc.subjectimmunohistochemistry
dc.subjectinflammation
dc.subjectkidney function
dc.subjectkidney injury
dc.subjectmale
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectplethysmography
dc.subjectprotein expression
dc.subjectrat
dc.subjectrenin angiotensin aldosterone system
dc.subjectrenovascular hypertension
dc.subjectsystolic blood pressure
dc.subjecturinary excretion fraction
dc.subjectWestern blotting
dc.subjectanimal
dc.subjectchemistry
dc.subjectdrug effect
dc.subjectgenetics
dc.subjecthuman
dc.subjectinjuries
dc.subjectkidney
dc.subjectkidney disease
dc.subjectpathology
dc.subjectPeumus boldus
dc.subjectrenovascular hypertension
dc.subjectAnimals
dc.subjectAporphines
dc.subjectHumans
dc.subjectHypertension, Renovascular
dc.subjectKidney
dc.subjectKidney Diseases
dc.subjectOxidative Stress
dc.subjectPeumus
dc.subjectRats
dc.subjectRenin-Angiotensin System
dc.subjectTransforming Growth Factor beta
dc.titleBoldine improves kidney damage in the goldblatt 2K1C model avoiding the increase in TGF-β
dc.typeArticle


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