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Open AccessArticle

Boldine Improves Kidney Damage in the Goldblatt 2K1C Model Avoiding the Increase in TGF-β

1
Departamento de Fisiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda #340, Santiago 8331150, Chile
2
Instituto de Ciencias Biomédicas, Facultad de Ciencias de la Salud, Universidad Autónoma de Chile, El Llano Subercaseaux #2801, Santiago 8910060, Chile
*
Authors to whom correspondence should be addressed.
Int. J. Mol. Sci. 2018, 19(7), 1864; https://doi.org/10.3390/ijms19071864
Received: 14 May 2018 / Revised: 15 June 2018 / Accepted: 19 June 2018 / Published: 25 June 2018
(This article belongs to the Special Issue Nutraceuticals in Cancer and Disease Prevention)
Boldine, 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. View Full-Text
Keywords: renovascular hypertension; chronic kidney disease; oxidative stress; fibrosis; (S)-2,9-dihydroxy-1,10-dimethoxy-aporphine renovascular hypertension; chronic kidney disease; oxidative stress; fibrosis; (S)-2,9-dihydroxy-1,10-dimethoxy-aporphine
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Gómez, G.I.; Velarde, V. Boldine Improves Kidney Damage in the Goldblatt 2K1C Model Avoiding the Increase in TGF-β. Int. J. Mol. Sci. 2018, 19, 1864.

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