Sodium hippurate, 98%

Sodium hippurate, 98% is an orally active metabolite. Sodium hippurate, 98% can be produced by intestinal microorganisms from the metabolism of polyphenols, benzoic acid. Sodium hippurate, 98% decreases NRF2, MMP9 and leads to ROS accumulation. Sodium hippurate, 98% activates TGFβ/SMAD signaling. Sodium hippurate, 98% improves hyperuricemia and colitis. Sodium hippurate, 98% can also be used in cardiovascular disease research^[1][2][3][4]. ^{[5][6][7][8][9]}. In Vitro:Sodium hippurate, 98% (Hippuric acid, 25 μM; 24 h) co-incubated with Dexamethasone (HY-14648) significantly increases C2C12 myotube diameter, abrogates dexamethasone-induced reductions in myotube protein synthesis rates, and partially attenuates the increase in proteolysis in C2C12 myotubes under atrophy-like conditions^[2].
Sodium hippurate, 98% (Hippuric acid, 1-2 mM; 15 min) significantly reduces P-selectin/CD62P expression and inhibits PAC-1 activation-dependant antibody expression in platelets stimulated ex vivo via the P₂Y₁/P₂Y₁₂-adenosine diphosphate (ADP) pathway^[3].
Sodium hippurate, 98% (Hippuric acid, 0-1000 μM; 24 h) increases fibrosis-related gene expression, extracellular matrix imbalance, and oxidative stress in HK-2 cells^[4].
Sodium hippurate, 98% (Hippuric acid, 200-400 ng/mL; 24 h) increases ABCG2 expression and apical localization in Caco-2 cells^[5].
Sodium hippurate, 98% (Hippuric acid, 8 mg/mL; 24 h) decreases pro-inflammatory cytokine production and promotes the expression of ZO-1 in NCM460 cells treated with dextran sulfate sodium^[6].
Sodium hippurate, 98% (Hippuric acid, concentration equivalent to that in 2.5% serum from blueberry-diet-fed rats) inhibits osteoclastogenesis and osteoclast resorptive activity in nonadherent mouse bone marrow cells isolated from 4-week-old C57BL6/J mice^[7].
In Vivo:Sodium hippurate, 98% (Hippuric acid, 100 mg/kg; i.p.; five times per week; 10 weeks) promotes renal fibrosis and dysfunction in 5/6 nephrectomized rats^[4].
Sodium hippurate, 98% (Hippuric acid, 10 mg/kg; p.o.; daily; 4 weeks) alleviates hyperuricemia in mice by promoting intestinal urate excretion via enhancing ABCG2-mediated transport^[5].
Sodium hippurate, 98% (Hippuric acid, 50-150 mg/kg; p.o.; once daily; 7 days) alleviates DSS-induced colitis in male C57BL/6J mice, as shown by reduced clinical activity, improved intestinal barrier integrity, and modulated gut microbiota^[6].