The Active Components of Sunflower (Helianthus annuus L.) Calathide and the Effects on Urate Nephropathy Based on COX-2/PGE2 Signaling Pathway and the Urate Transporter URAT1, ABCG2, and GLUT9

The sunflower (Helianthus annuus L.) calathide is gradually used as an alternative treatment for hyperuricemia; nevertheless, evidence regarding its main components and therapeutic capacity for urate nephropathy is lacking. Identification of sunflower calathide aqueous extract (SCE) was rapidly done by UPLC-ESI-Q-Orbitrap, and 32 water-soluble compounds with a comprehensive score >80 were discovered. Besides, yeast extract was administrated to induce high UA levels and hyperuricemic renal injury. We found that SCE treatment not only decreased UA levels to a comparable degree as allopurinol and benzbromarone, but also reduced the BUN levels and participated in kidney injury repair induced by uric acid. Moreover, it regulated the expression of URAT1 and ABCG2, especially inhibiting the GLUT9 in the normal kidney. Results were multifacetedly evaluated with a view to suggesting a possible mechanism of action as compared with those of allopurinol and benzbromarone by western blotting, H&E staining, and immunohistochemistry. However, the H&E staining showed histological changes in model, benzbromarone, and allopurinol groups rather than SCE treatments, and at the same time, the uric acid was identified as a cause of renal damage. The antiinflammatory effects and the regulations of COX-2/PGE2 signaling pathway were revealed on the LPS-induced RAW264.7 cells, indicating that the SCE not only increased cellular proliferation but also downregulated the COX-2, PGE2, NO, and IFN-γ cytokines in the RAW264.7 cells. To conclude, the SCE acts on urate transporters and contributes to prevent urate nephropathy via alleviating inflammatory process involving COX-2/PGE2 signaling pathway. It is available to develop SCE as food supplemental applications for hyperuricemia and nephritic inflammation.

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Association of Hyperuricemia With Acute Kidney Injury: Case Series Report Among Patients Hospitalized With General Tonic-Clonic Seizures

Canadian Journal of Kidney Health and Disease ◽

10.1177/2054358120977386 ◽

2020 ◽

Vol 7 ◽

pp. 205435812097738

Author(s):

Jean Maxime Côté ◽

Arline-Aude Bérubé ◽

Guillaume Bollée

Keyword(s):

Acute Kidney Injury ◽

Uric Acid ◽

Serum Creatinine ◽

Serum Uric Acid ◽

Case Series ◽

Kidney Injury ◽

Clonic Seizure ◽

Tonic Clonic Seizure ◽

Median Serum ◽

Urate Nephropathy

Background: Urate nephropathy is a rare cause of acute kidney injury. Although most risk factors are associated with chemotherapy, tumor lysis syndrome or rhabdomyolysis, occurrence following severe seizure has also been reported. Uric acid measurement following convulsion is rarely performed and, therefore, the incidence of hyperuricemia in this context is unknown. Objective: The objective is to present a case of urate nephropathy following generalized tonic-clonic seizure (GTCS) and to investigate the kinetics of serum uric acid and creatinine levels in a series of patients admitted for severe seizures. Design: Retrospective case report and prospective case series. Setting: Emergency room department and neurology unit of a tertiary care hospital. Patients: The study included 13 hospitalized patients for severe GTCS. Measurements: Type, timing, and duration of seizure episodes were documented. Demographic data, weight, hypouricemic therapy, and baseline serum creatinine were recorded. Blood samples (uric acid, creatinine, blood gas, lactate, and creatinine kinase) and urine samples (uric acid, creatinine, and dipstick) were prospectively collected at Day 0, 1, 2, and 3 following the GTCS episode. Methods: We identified and described one rare case of urate nephropathy following GTCS. Then, we presented the kinetic of uric acid and creatinine levels and the acute kidney injury incidence over the follow-up period. All analyses were using descriptive statistics. Results: During the study period, 13 patients with a median tonic-clonic seizure duration of 5.0 minutes (interquartile range [IQR], 2.0–12.5) were included. From day 0 to day 3, the median serum uric acid level decreased from 346.0 µmol/L (IQR, 155.0–377.5) to 178.0 µmol/L (IQR, 140.0–297.5) and median serum creatinine from 73.0 µmol/L (IQR, 51.0–80.0) to 57.0 µmol/L (IQR, 44.0–70.0). Acute kidney injury occurred in four patients. Limitations: This is a single-center observational study with small sample size, which does not allow us to demonstrate causality between the increase of uric acid levels observed and the occurrence of acute kidney injury. A delay between the first sampling and seizure episodes was observed and could explain the limited increase of uric acid levels captured. Conclusions: There is a signal for an acute increase of uric acid levels following a severe seizure before returning to baseline within 3 days. During that period, there might be an increased risk of acute kidney injury, although these changes seem to be usually mild and reversible. Our findings suggest that routine serum uric acid measurement in patients presenting with GTCS could help to identify those patients at risk of developing acute kidney injury as a result of acute hyperuricemia. Further larger studies are required to confirm the effectiveness of such screening in acute kidney injury prevention. Trial Registration: As an observational noninterventional study, no registration was required.

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Anti-Inflammatory Effects of Berchemia floribunda in LPS-Stimulated RAW264.7 Cells through Regulation of NF-κB and MAPKs Signaling Pathway

Plants ◽

10.3390/plants10030586 ◽

2021 ◽

Vol 10 (3) ◽

pp. 586

Author(s):

Hyun Ji Eo ◽

Jun Hyuk Jang ◽

Gwang Hun Park

Keyword(s):

Signaling Pathway ◽

Inflammatory Activity ◽

Nuclear Accumulation ◽

Raw264.7 Cells ◽

No Production ◽

Tnf Α ◽

Inflammatory Drugs ◽

Cox 2 ◽

Anti Inflammatory ◽

Inflammatory Effect

Berchemia floribunda (Wall.) Brongn. (BF), which belongs to Rhamnaceae, is a special plant of Anmyeon Island in Korea. BF has been reported to have antioxidant and whitening effects. However, the anti-inflammatory activity of BR has not been elucidated. In this study, we evaluated the anti-inflammatory effect of leaves (BR-L), branches (BR-B) and fruit (BR-F) extracted with 70% ethanol of BR and elucidated the potential signaling pathway in LPS-induced RAW264.7 cells. BR-L showed a strong anti-inflammatory activity through the inhibition of NO production. BR-L significantly suppressed the production of the pro-inflammatory mediators such as iNOS, COX-2, IL-1β, IL-6 and TNF-α in LPS-stimulated RAW264.7 cells. BR-L suppressed the degradation and phosphorylation of IκB-α, which contributed to the inhibition of p65 nuclear accumulation and NF-κB activation. BR-L obstructed the phosphorylation of MAPKs (ERK1/2, p38 and JNK) in LPS-stimulated RAW264.7 cells. Consequently, these results suggest that BR-L may have great potential for the development of anti-inflammatory drugs to treat acute and chronic inflammatory disorders.

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Two cases of acute urate nephropathy in women with asymptomatic hyperuricemia

Rheumatology Science and Practice ◽

10.47360/1995-4484-2021-103-107 ◽

2021 ◽

Vol 59 (1) ◽

pp. 103-107

Author(s):

L. N. Yeliseyeva ◽

V. P. Kurinnaya ◽

O. N. Ponkina ◽

I. V. Semizarova ◽

Z. A. Baste

Keyword(s):

Acute Kidney Injury ◽

Uric Acid ◽

Serum Uric Acid ◽

Clinical Manifestations ◽

Kidney Injury ◽

Pathological Examination ◽

Biopsy Material ◽

Morphological Picture ◽

Urate Nephropathy

The article presents a description of two own observations of the development of acute urate nephropathy in women with asymptomatic hyperuricemia. Clinical data and the results of additional laboratory and instrumental studies are presented; in one of the observations, the morphological picture of intravital biopsy material against the background of prolonged use of diuretics is described. The second case characterizes tophus kidney damage (according to the pathological examination data) without characteristic clinical manifestations of gout in vivo. The authors draw attention to the need to study serum uric acid levels in all cases of acute kidney injury.

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Mulberry leaf active components alleviate type 2 diabetes and its liver and kidney injury in db/db mice through insulin receptor and TGF-β/Smads signaling pathway

Biomedicine & Pharmacotherapy ◽

10.1016/j.biopha.2019.108675 ◽

2019 ◽

Vol 112 ◽

pp. 108675 ◽

Cited By ~ 6

Author(s):

Liwen Zhang ◽

Shulan Su ◽

Yue Zhu ◽

Jianming Guo ◽

Sheng Guo ◽

...

Keyword(s):

Type 2 Diabetes ◽

Insulin Receptor ◽

Signaling Pathway ◽

Kidney Injury ◽

Active Components ◽

Mulberry Leaf ◽

Liver And Kidney

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Changes in Water Soluble Uremic Toxins and Urinary Acute Kidney Injury Biomarkers After 10- and 100-km Runs

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph16214153 ◽

2019 ◽

Vol 16 (21) ◽

pp. 4153 ◽

Cited By ~ 4

Author(s):

Wołyniec ◽

Kasprowicz ◽

Giebułtowicz ◽

Korytowska ◽

Zorena ◽

...

Keyword(s):

Acute Kidney Injury ◽

Uric Acid ◽

Kidney Injury ◽

Uremic Toxins ◽

Water Soluble ◽

Post Exercise ◽

Neutrophil Gelatinase Associated Lipocalin ◽

Before And After ◽

Kidney Injury Molecule 1 ◽

Neutrophil Gelatinase

Acute kidney injury (AKI) is described as a relatively common complication of exercise. In clinical practice the diagnosis of AKI is based on serum creatinine, the level of which is dependent not only on glomerular filtration rate but also on muscle mass and injury. Therefore, the diagnosis of AKI is overestimated after physical exercise. The aim of this study was to determine changes in uremic toxins: creatinine, urea, uric acid, asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA), trimethylamine N-oxide (TMAO) and urinary makers of AKI: albumin, neutrophil gelatinase-associated lipocalin (uNGAL), kidney injury molecule-1 and cystatin-C (uCyst-C) after long runs. Sixteen runners, mean age 36.7 ± 8.2 years, (2 women, 14 men) participating in 10- and 100-km races were studied. Blood and urine were taken before and after the races to assess markers of AKI. A statistically significant increase in creatinine, urea, uric acid, SDMA and all studied urinary AKI markers was observed. TMAO and ADMA levels did not change. The changes in studied markers seem to be a physiological reaction, because they were observed almost in every runner. The diagnosis of kidney failure after exercise is challenging. The most valuable novel markers which can help in post-exercise AKI diagnosis are uCyst-C and uNGAL.

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Restrictive fluid regimen in combination with COX-2 inhibitors in open pancreatic surgery increases risk of postoperative acute kidney injury

10.26226/morressier.57108e30d462b80290b4a85d ◽

2016 ◽

Author(s):

Andreas Abrahamsson

Keyword(s):

Acute Kidney Injury ◽

Pancreatic Surgery ◽

Kidney Injury ◽

Fluid Regimen ◽

Cox 2 ◽

Cox 2 Inhibitors

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Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽

10.3390/molecules25163573 ◽

2020 ◽

Vol 25 (16) ◽

pp. 3573

Author(s):

Lian-Chun Li ◽

Zheng-Hong Pan ◽

De-Sheng Ning ◽

Yu-Xia Fu

Keyword(s):

Nitric Oxide ◽

Signaling Pathway ◽

Morphological Changes ◽

Raw264.7 Cells ◽

Enzyme Linked Immunosorbent Assay ◽

Tnf Α ◽

Anti Inflammatory ◽

Factor Α ◽

Oxide Synthase ◽

Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

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