Is there anything good in uric acid?

Álvarez-Lario, Bonifacio; Macarrón-Vicente, Jesús

doi:10.1093/qjmed/hcr159

Cited by 113 publications

(98 citation statements)

References 82 publications

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“…High physiological UA levels in humans and higher primates have been hypothesized to be protective against oxidative stress [18, 19]. However, a series of well-grounded epidemiological studies have demonstrated the association between high serum UA levels and increased risk for a variety of diseases [20-23].…”

Section: Discussionmentioning

confidence: 99%

Uric Acid Induces Cardiomyocyte Apoptosis via Activation of Calpain-1 and Endoplasmic Reticulum Stress

Yan

Chen

et al. 2018

Cell Physiol Biochem

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Background/Aims: Hyperuricemia is associated with an increased risk for multiple cardiovascular diseases, but the underlying mechanisms remain largely elusive. Calpain-1 is a protease that is implicated in several pathological conditions that affect the heart. The aim of this current study was to test the effects of uric acid (UA) on cardiomyocyte survival and cardiac function and to investigate the role of calpain-1 in the UA-induced effects in the heart and their underlying mechanisms. Methods: In vivo, hyperuricemia was induced by oxonic acid (OA) administration in Sprague-Dawley rats for 16 weeks; TUNEL staining was used to identify apoptotic cells. Left ventricular (LV) sections were stained with Sirius Red to evaluate interstitial fibrosis. Cardiac catheterization was performed to evaluate cardiac function. In vitro, cultured H9c2 cells were incubated with different UA concentrations. MTT assays and flow cytometry were used to evaluate cell viability and apoptosis. All related gene expression levels were analyzed by quantitative real-time PCR (qRT-PCR), and all protein expression levels were analyzed by western blotting. Results: Hyperuricemia induction in vivo resulted in cellular apoptosis, interstitial fibrosis and diastolic dysfunction in the rat hearts, as well as increased activation of calpain-1 and endoplasmic reticulum (ER) stress, while allopurinol treatment mitigated the above changes. UA administration in vitro increased apoptosis and decreased H9c2 cell viability in a dose-dependent manner. Increased activation of calpain-1 and ER stress was also observed in the groups with high UA levels. Calpain-1 siRNA and the calpain inhibitor CI-III alleviated UA-induced ER stress and apoptosis, while inhibiting ER stress by tauroursodeoxycholic acid (TUDCA) mitigated UA-induced apoptosis without affecting calpain-1 expression or activity. Conclusions: These findings suggest that UA induces cardiomyocyte apoptosis through activation of calpain-1 and ER stress. These results may provide new insights into the mechanisms of hyperuricemia-associated cardiovascular risks and hopefully identify new treatment targets.

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Section: Discussionmentioning

confidence: 99%

Uric Acid Induces Cardiomyocyte Apoptosis via Activation of Calpain-1 and Endoplasmic Reticulum Stress

Yan

Chen

et al. 2018

Cell Physiol Biochem

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“…Recent studies demonstrated that hyperuricemia is linked not only to gout but also to other important disorders including hypertension, chronic kidney disease, cardiovascular disease, and metabolic syndrome [29]. Prior to considering a drug treatment for symptoms, adopting a progressive life style change such as healthier eating habits is considered important for the prevention and treatment of hyperuricemia [30].…”

Section: Discussionmentioning

confidence: 99%

Beneficial effects of rice endosperm protein intake in Japanese men with risk factors for metabolic syndrome: a randomized, crossover clinical trial

Hosojima

Kaseda

Kondo³

et al. 2016

BMC Nutr

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Background: Rice protein is proved to have hypocholesterolemic and anti-atherosclerotic effects, and a few experimental studies showed its renoprotective effects, using animal diabetic models. However, no clinical studies have investigated its benefits for human health. We aimed to clarify how the intake of rice endosperm protein affects markers correlating to lipid dysfunction in human. Methods: We recruited 18 male volunteers, 26-64 years of age, with risk factors for metabolic syndrome and allocated randomly into two groups. Half of them were administered test food containing rice endosperm protein and other half were administered control food containing sodium caseinate for 4 weeks. The dose of supplemental protein was 10 g/day. After medical examinations, the study foods were switched and the intervention was continued for another 4 weeks. Lipid metabolism markers were evaluated as primary outcome measures. Cross-over analysis was performed for 18 subjects using physical and clinical values measured before and after each intervention period.

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“…However, as Alvarez-Lario said (Alvarez, Macarrón, 2011), if UA was a waste or harmful product, it poorly explained why our kidneys recover 90% of filtered UA, instead of eliminating it. In fact, UA as a natural antioxidant plays an important role not only on induction of inflammatory response but also on anti-oxidative stress in peripheral and central tissue (Glantzounis et al, 2005).…”

Section: Introductionmentioning

confidence: 89%

Relationship between oxidative stress and inflammation in peripheral and cerebral system of oxonate-induced hyperuricemic rats

Zhong

Ping

et al. 2018

Braz. J. Pharm. Sci.

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To study what kind of role uric acid play on the relationship between oxidative Stress and inflammation in peripheral and cerebral system of oxonate-induced hyperuricemic rats. Twenty-six eight male Wistar rats were divided into two groups randomly. Potassium oxonate was used to establish hyperuricemic model for four weeks. In 2 nd and 4 th week, uric acid (UA) level, total superoxide dismutase (T-SOD), Gu,Zn-SOD activity and interleukin-1beta (IL-1β) concentration in serum were determined respectively. In 4 th week, one hour after last PO treatment, five rats of every group were given Evans Blue to test blood-brain barrier (BBB) permeability. Other brains were obtained to analysis T-SOD, Gu,Zn-SOD activity and IL-1β concentration in cerebral system. Meanwhile, brain and kidney were stained with hematoxylin and eosin (H&E) to observe pathological change. In 2 nd week, both of T-SOD and Gu,Zn-SOD activity in serum increased obviously (P<0.05) in hyperuricemia rats. However, IL-1β content didn't change remarkably. In the 4 th week, T-SOD activity in model group had become similar with control group, and at the same time IL-1β content in serum increased significantly (P<0.05). Pathological section showed the structural and functional unit of the kidney had been damaged. On the contrary, both of T-SOD and Gu,Zn-SOD activity in brain increased obviously (P<0.05), but IL-1β concentration was no significant difference between two groups. In addition, the results of Evans Blue and H&E suggested the integrity of BBB and structure of brain were not changed after PO treatment. The permeability of BBB and form of UA would be potential factors to decide what kind role UA play on keeping balance between antioxidative stress and induction of inflammatory response.

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Is there anything good in uric acid?

Cited by 113 publications

References 82 publications

Uric Acid Induces Cardiomyocyte Apoptosis via Activation of Calpain-1 and Endoplasmic Reticulum Stress

Uric Acid Induces Cardiomyocyte Apoptosis via Activation of Calpain-1 and Endoplasmic Reticulum Stress

Beneficial effects of rice endosperm protein intake in Japanese men with risk factors for metabolic syndrome: a randomized, crossover clinical trial

Relationship between oxidative stress and inflammation in peripheral and cerebral system of oxonate-induced hyperuricemic rats

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