2012
DOI: 10.1016/j.jep.2011.11.032
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Protective effects of Eucommia lignans against hypertensive renal injury by inhibiting expression of aldose reductase

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Cited by 26 publications
(24 citation statements)
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“…Our results indicated that both FER and ZOP significantly reduced the elevations in diastolic BP associated with MetS. The effect of FER is explained by its AR inhibition, which is consistent with previous studies that reported that AR inhibition protects against development of hypertension in spontaneously hypertensive rat [26] and diabetic rat [27] models.…”
Section: Discussionsupporting
confidence: 92%
“…Our results indicated that both FER and ZOP significantly reduced the elevations in diastolic BP associated with MetS. The effect of FER is explained by its AR inhibition, which is consistent with previous studies that reported that AR inhibition protects against development of hypertension in spontaneously hypertensive rat [26] and diabetic rat [27] models.…”
Section: Discussionsupporting
confidence: 92%
“…Eucommia extract was shown to possess antioxidative effect [12, 13], hypoglycemic and hypolipidemic effects [14, 15], and antihypertensive effect [16, 17]. Lignans, the major bioactive compounds of Eucommia , was shown to inhibit hypertensive renal injury [18] and angiotensin II induced proliferation [19, 20] and extracellular matrix production [20] in rat mesangial cells. This study aimed to investigate whether PD has protective effects against oxLDL-induced endothelial dysfunction.…”
Section: Introductionmentioning
confidence: 99%
“…We previously confirmed that lignans were the effective fraction of Du-zhong for antihypertension [10,19]. Further study showed that both N-acetyl-β-D-glucosaminidase enzyme activity and the ratio of albumin to urinary creatinine decreased in spontaneous hypertensive rat (SHR)-treated with Eucommia lignans [12]. Eucommia lignans also inhibited the expression of collagen type III (Col III) in the glomerular basement membrane, and diminished the over-expression of AR in the kidney [11].…”
Section: Introductionmentioning
confidence: 90%
“…AR can be activated by TGF-β1, oxidative stress and inflammation [9-12], to stimulate proliferation of MCs and deposition of ECM induced by TGF-β1 and PDGF [13-16]. An over-expression of AR was observed in the renal tissue of spontaneous hypertensive rats (SHR) in our previous study [12]. AR might be involved in the pathological process induced by Ang II in MCs.…”
Section: Introductionmentioning
confidence: 99%
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