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Glucosyl hesperidin prevents endothelial dysfunction and oxidative stress in spontaneously hypertensive rats.
Nutrition. 2008 May; 24(5):470-6.N

Abstract

OBJECTIVE

Glucosyl hesperidin (G-hesperidin), a water-soluble hesperidin derivative, has antihypertensive effects. A detailed understanding of the mechanism of the blood pressure-lowering effect, however, remains obscure. The aim of this work was to investigate the underlying mechanisms involved in the hypotensive effect of G-hesperidin in spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto rats (WKYs).

METHODS

Fourteen-week-old SHRs and WKYs were fed a control or G-hesperidin (50 mg/kg) diet for 8 wk. Blood pressure was recorded weekly. After 8 wk, the vasodilatory responses of isolated aortas to acetylcholine and sodium nitroprusside were assessed. Expression of mRNAs related to regulation of blood pressure and vascular tone in the aorta also was investigated. Urinary 8-hydroxy-2'-deoxyguanosine, an oxidative stress marker, was measured. Cardiac and vascular hypertrophies were observed.

RESULTS

In SHRs, the ingestion of G-hesperidin inhibited the development of hypertension. G-hesperidin enhanced endothelium-dependent vasodilation in response to acetylcholine, but had no effect on endothelium-independent vasodilation in response to sodium nitroprusside. G-hesperidin decreased mRNA expression of nicotinamide adenine dinucleotide phosphate oxidase subunits in aorta, which are the main source of superoxide anion in the vasculature; endothelial nitric oxide synthase expression was unchanged. Urinary 8-hydroxy-2'-deoxyguanosine was reduced significantly by G-hesperidin treatment. G-hesperidin suppressed cardiac and vascular hypertrophies. In contrast, G-hesperidin had no effects in WKYs.

CONCLUSION

Continuous ingestion of G-hesperidin reduces oxidative stress by inhibiting nicotinamide adenine dinucleotide phosphate oxidase expression in the vasculature, thereby ameliorating endothelial dysfunction and hypertension in SHRs.

Authors+Show Affiliations

Biological Science Laboratories, Kao Corporation, Tochigi, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18329851

Citation

Yamamoto, Masaki, et al. "Glucosyl Hesperidin Prevents Endothelial Dysfunction and Oxidative Stress in Spontaneously Hypertensive Rats." Nutrition (Burbank, Los Angeles County, Calif.), vol. 24, no. 5, 2008, pp. 470-6.
Yamamoto M, Suzuki A, Jokura H, et al. Glucosyl hesperidin prevents endothelial dysfunction and oxidative stress in spontaneously hypertensive rats. Nutrition. 2008;24(5):470-6.
Yamamoto, M., Suzuki, A., Jokura, H., Yamamoto, N., & Hase, T. (2008). Glucosyl hesperidin prevents endothelial dysfunction and oxidative stress in spontaneously hypertensive rats. Nutrition (Burbank, Los Angeles County, Calif.), 24(5), 470-6. https://doi.org/10.1016/j.nut.2008.01.010
Yamamoto M, et al. Glucosyl Hesperidin Prevents Endothelial Dysfunction and Oxidative Stress in Spontaneously Hypertensive Rats. Nutrition. 2008;24(5):470-6. PubMed PMID: 18329851.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glucosyl hesperidin prevents endothelial dysfunction and oxidative stress in spontaneously hypertensive rats. AU - Yamamoto,Masaki, AU - Suzuki,Atsushi, AU - Jokura,Hiroko, AU - Yamamoto,Naoki, AU - Hase,Tadashi, Y1 - 2008/03/10/ PY - 2007/08/30/received PY - 2007/12/21/revised PY - 2008/01/20/accepted PY - 2008/3/11/pubmed PY - 2008/8/12/medline PY - 2008/3/11/entrez SP - 470 EP - 6 JF - Nutrition (Burbank, Los Angeles County, Calif.) JO - Nutrition VL - 24 IS - 5 N2 - OBJECTIVE: Glucosyl hesperidin (G-hesperidin), a water-soluble hesperidin derivative, has antihypertensive effects. A detailed understanding of the mechanism of the blood pressure-lowering effect, however, remains obscure. The aim of this work was to investigate the underlying mechanisms involved in the hypotensive effect of G-hesperidin in spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto rats (WKYs). METHODS: Fourteen-week-old SHRs and WKYs were fed a control or G-hesperidin (50 mg/kg) diet for 8 wk. Blood pressure was recorded weekly. After 8 wk, the vasodilatory responses of isolated aortas to acetylcholine and sodium nitroprusside were assessed. Expression of mRNAs related to regulation of blood pressure and vascular tone in the aorta also was investigated. Urinary 8-hydroxy-2'-deoxyguanosine, an oxidative stress marker, was measured. Cardiac and vascular hypertrophies were observed. RESULTS: In SHRs, the ingestion of G-hesperidin inhibited the development of hypertension. G-hesperidin enhanced endothelium-dependent vasodilation in response to acetylcholine, but had no effect on endothelium-independent vasodilation in response to sodium nitroprusside. G-hesperidin decreased mRNA expression of nicotinamide adenine dinucleotide phosphate oxidase subunits in aorta, which are the main source of superoxide anion in the vasculature; endothelial nitric oxide synthase expression was unchanged. Urinary 8-hydroxy-2'-deoxyguanosine was reduced significantly by G-hesperidin treatment. G-hesperidin suppressed cardiac and vascular hypertrophies. In contrast, G-hesperidin had no effects in WKYs. CONCLUSION: Continuous ingestion of G-hesperidin reduces oxidative stress by inhibiting nicotinamide adenine dinucleotide phosphate oxidase expression in the vasculature, thereby ameliorating endothelial dysfunction and hypertension in SHRs. SN - 0899-9007 UR - https://www.unboundmedicine.com/medline/citation/18329851/Glucosyl_hesperidin_prevents_endothelial_dysfunction_and_oxidative_stress_in_spontaneously_hypertensive_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0899-9007(08)00033-6 DB - PRIME DP - Unbound Medicine ER -