Baocai Fu’s scientific contributions

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Publications (2)


Effects of H2O2 exposure on PE- and KCl-induced contraction in rat aortic rings. (a) KCl induced contractile response in H2O2-treated aortic rings with (E+) or without (E−) endothelium. (b) PE induced contractile response in H2O2-treated aortic rings with (E+) or without (E−) endothelium. (c) ACh induced vasodilative response in H2O2-treated rat aorta with intact endothelium. (d) 5.0 mM H2O2 pulse treatment (10 min) induced the endothelium-dependent vasodilation impairments in rat aortic rings with intact endothelium. Data represents as means ± SD (n=6). (a and b) ∗P<0.05, ∗∗P<0.01 versus the respective untreated group; ##P<0.01 versus the endothelium-intact aortic rings treated with the same concentration of H2O2; (c and d) ∗∗P<001 versus the untreated group.
Effects of H2O2 exposure on PE- and KCl-induced contraction in rat aortic rings. (a) KCl induced contractile response in H2O2-treated aortic rings with (E+) or without (E−) endothelium. (b) PE induced contractile response in H2O2-treated aortic rings with (E+) or without (E−) endothelium. (c) ACh induced vasodilative response in H2O2-treated rat aorta with intact endothelium. (d) 5.0 mM H2O2 pulse treatment (10 min) induced the endothelium-dependent vasodilation impairments in rat aortic rings with intact endothelium. Data represents as means ± SD (n=6). (a and b) ∗P<0.05, ∗∗P<0.01 versus the respective untreated group; ##P<0.01 versus the endothelium-intact aortic rings treated with the same concentration of H2O2; (c and d) ∗∗P<001 versus the untreated group.
Effects of H2O2 exposure on PE- and KCl-induced contraction in rat aortic rings. (a) KCl induced contractile response in H2O2-treated aortic rings with (E+) or without (E−) endothelium. (b) PE induced contractile response in H2O2-treated aortic rings with (E+) or without (E−) endothelium. (c) ACh induced vasodilative response in H2O2-treated rat aorta with intact endothelium. (d) 5.0 mM H2O2 pulse treatment (10 min) induced the endothelium-dependent vasodilation impairments in rat aortic rings with intact endothelium. Data represents as means ± SD (n=6). (a and b) ∗P<0.05, ∗∗P<0.01 versus the respective untreated group; ##P<0.01 versus the endothelium-intact aortic rings treated with the same concentration of H2O2; (c and d) ∗∗P<001 versus the untreated group.
Effects of H2O2 exposure on PE- and KCl-induced contraction in rat aortic rings. (a) KCl induced contractile response in H2O2-treated aortic rings with (E+) or without (E−) endothelium. (b) PE induced contractile response in H2O2-treated aortic rings with (E+) or without (E−) endothelium. (c) ACh induced vasodilative response in H2O2-treated rat aorta with intact endothelium. (d) 5.0 mM H2O2 pulse treatment (10 min) induced the endothelium-dependent vasodilation impairments in rat aortic rings with intact endothelium. Data represents as means ± SD (n=6). (a and b) ∗P<0.05, ∗∗P<0.01 versus the respective untreated group; ##P<0.01 versus the endothelium-intact aortic rings treated with the same concentration of H2O2; (c and d) ∗∗P<001 versus the untreated group.
Rosmarinic acid alleviates the endothelial dysfunction induced by H2O2 in endothelium-intact rat aortic rings. (a) Rosmarinic acid (RA) pulse exposure showed no effect on the contraction induced by KCl in rat aortic rings. (b) Rosmarinic acid (RA) pulse exposure showed no effect on the contraction induced by PE in rat aortic rings. (c) Rosmarinic acid (RA) preincubation alleviated the endothelium-dependent vasodilation impairments induced by H2O2. (d) Rosmarinic acid (RA) cotreatment inhibited the NBT reduction induced by H2O2 in the endothelium-intact aortic rings. The results were expressed as the means ± SD (n=6). ∗∗P<0.01 versus the untreated control group; ##P<001 versus the H2O2-treated group.

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Rosmarinic Acid Alleviates the Endothelial Dysfunction Induced by Hydrogen Peroxide in Rat Aortic Rings via Activation of AMPK
  • Article
  • Full-text available

August 2017

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75 Reads

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23 Citations

Hui Zhou

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Baocai Fu

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Bo Xu

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Endothelial dysfunction is the key player in the development and progression of vascular events. Oxidative stress is involved in endothelial injury. Rosmarinic acid (RA) is a natural polyphenol with antioxidative, antiapoptotic, and anti-inflammatory properties. The present study investigates the protective effect of RA on endothelial dysfunction induced by hydrogen peroxide (H 2 O 2 ). Compared with endothelium-denuded aortic rings, the endothelium significantly alleviated the decrease of vasoconstrictive reactivity to PE and KCl induced by H 2 O 2 . H 2 O 2 pretreatment significantly injured the vasodilative reactivity to ACh in endothelium-intact aortic rings in a concentration-dependent manner. RA individual pretreatment had no obvious effect on the vasoconstrictive reaction to PE and KCl, while its cotreatment obviously mitigated the endothelium-dependent relaxation impairments and the oxidative stress induced by H 2 O 2 . The RA cotreatment reversed the downregulation of AMPK and eNOS phosphorylation induced by H 2 O 2 in HAEC cells. The pretreatment with the inhibitors of AMPK (compound C) and eNOS (L-NAME) wiped off RA’s beneficial effects. All these results demonstrated that RA attenuated the endothelial dysfunction induced by oxidative stress by activating the AMPK/eNOS pathway.

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Citations (1)


... The protective effects of RA on rat renal IRI reduced serum parameters (creatinine and BUN), the level of MDA, and safeguarded the kidney tissue from adverse histopathological changes [39]. Rosmarinic acid reduces oxidative stress-induced endothelial dysfunction by stimulating the AMPK/eNOS pathway [40]. In kidney disorders, endothelial dysfunction is associated with reduced NO production as a result of decreased eNOS expression or activity [41]. ...

Reference:

Rosmarinic acid: a promising agent for male rats’ renal protection against ischemia/reperfusion injury
Rosmarinic Acid Alleviates the Endothelial Dysfunction Induced by Hydrogen Peroxide in Rat Aortic Rings via Activation of AMPK