Hyperuricemia, endothelial dysfunction and hypertension

Miricescu, Daniela; Pharmacy, Bucharest; Totan, Alexandra; Ştefani, Constantin; Stănescu, Iulia-Ioana; Imre, Marina; Stănescu, Ana Maria Alexandra; Rădulescu, Radu; Bălan, Daniela Gabriela; Balcangiu‐Stroescu, Andra-Elena; Greabu, Maria

doi:10.37897/rjmp.2020.2.10

Cited by 1 publication

(1 citation statement)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…While oxidative stress responses can activate inflammatory factors in kidney cells and induce innate immune responses in vivo, the activation of related proinflammatory factors induces the development of inflammation [7][8][9]. Hyperuricemia has been reported to be closely related to oxidative stress and inflammatory responses [10]. At present, the drugs for the treatment of HUA in clinical practice including allopurinol, benzbromarone, and sodium bicarbonate can control the level of uric acid, but they have a series of toxic side effects such as liver and kidney function injury and hematopoietic dysfunction [11,12].…”

Section: Introductionmentioning

confidence: 99%

Inflammatory Response and Oxidative Stress as Mechanism of Reducing Hyperuricemia of Gardenia jasminoides‐Poria cocos with Network Pharmacology

Liu

Jiang

Liu

et al. 2021

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Hyperuricemia (HUA) is a metabolic disease, closely related to oxidative stress and inflammatory responses, caused by reduced excretion or increased production of uric acid. However, the existing therapeutic drugs have many side effects. It is imperative to find a drug or an alternative medicine to effectively control HUA. It was reported that Gardenia jasminoides and Poria cocos could reduce the level of uric acid in hyperuricemic rats through the inhibition of xanthine oxidase (XOD) activity. But there were few studies on its mechanism. Therefore, the effective ingredients in G. jasminoides and P. cocoa extracts (GPE), the active target sites, and the further potential mechanisms were studied by LC-/MS/MS, molecular docking, and network pharmacology, combined with the validation of animal experiments. These results proved that GPE could significantly improve HUA induced by potassium oxazine with the characteristics of multicomponent, multitarget, and multichannel overall regulation. In general, GPE could reduce the level of uric acid and alleviate liver and kidney injury caused by inflammatory response and oxidative stress. The mechanism might be related to the TNF-α and IL-7 signaling pathway.

show abstract