ABSTRACT
BACKGROUND: Diabetic kidney disease (DKD) is among the most important causes for chronic kidney disease. Anthocyanins (ANT) are polyphenolic compounds present in various food and play an important role in ameliorating hyperglycemia and insulin sensitivity. However, the effects of ANT in DKD are still poorly understood. This study aimed to investigate the effect of ANT (cyanidin-3-O-glucoside [C3G]) on the renal function of DKD, and whether the anti-DKD effect of ANT is related to metabolic pathways. METHODS: To explore the role of ANT in DKD, we performed the examination of blood glucose, renal function, and histopathology. As for the mechanism, we designed the label-free quantification proteomics and nontargeted metabolomics analysis for kidney and serum. Subsequently, we revealed the anti-DKD effect of ANT through the bioinformatic analysis. RESULTS: We showed that the fasting blood glucose level (- 6.1 mmol/L, P = 0.037), perimeter of glomerular lesions (- 24.1 µm, P = 0.030), fibrosis score of glomerular (- 8.8%, P = 0.002), and kidney function (Cystatin C: - 701.4 pg/mL, P = 0.043; urine creatinine: - 701.4 mmol/L, P = 0.032) were significantly alleviated in DKD mice after ANT treatment compared to untreated in the 20th week. Further, proteins and metabolites in the kidneys of DKD mice were observed to be dramatically altered due to changes in amino acid metabolism with ANT treatment; mainly, taurine and hypotaurine metabolism pathway was upregulated (P = 0.0001, t value = 5.97). Furthermore, upregulated tryptophan metabolism (P < 0.0001, t value = 5.94) and tyrosine metabolism (P = 0.0037, t value = 2.91) pathways had effects on serum of DKD mice as responsed ANT regulating. CONCLUSIONS: Our results suggested that prevention of the progression of DKD by ANT could be related to the regulation of amino acid metabolism. The use of dietary ANT may be one of the dietary strategies to prevent and treat DKD.
Subject(s)
Diabetes Mellitus , Diabetic Nephropathies , Mice , Animals , Diabetic Nephropathies/metabolism , Anthocyanins/pharmacology , Anthocyanins/therapeutic use , Blood Glucose , Kidney/pathology , Amino Acids , Diabetes Mellitus/pathologyABSTRACT
In the title compound, [Zn(2)(C(36)H(42)N(4)O(2))(CH(3)COO)(2)]·2CH(3)CH(2)OH, a centrosymmetric dinuclear zinc macrocyclic complex is accompanied by two half-occupied ethanol solvent molecues resulting in a 1:2 macrocycle-solvent composition. The Zn(II) atom has a square-pyramidal geometry arising from an N(2)O(3) donor set, being coordinated by two N atoms and two O atoms from the macrocyclic ligand in the equatorial sites and one O atom from an acetate anion in the apical site. The two Zn(II) atoms are linked by two phenolate O atoms, generating a four-membered Zn(2)O(2) ring at the centre of the macrocycle. The tert-butyl group shows rotational disorder over two sets of sites in a 0.552â (12):0.448â (12) ratio. In the crystal, N-Hâ¯O and O-Hâ¯O hydrogen bonds are seen and a short intra-molecular C-Hâ¯O contact occurs.
ABSTRACT
In the title centrosymmetric dinuclear zinc(II) complex, [Zn(2)(C(36)H(42)N(4)O(2))(NO(3))(2)], the Zn(II) atom has a distorted octa-hedral geometry, defined by two N atoms and two O atoms from the macrocyclic ligand and two O atoms from a chelating nitrate anion and are bridged by two phenolate O atoms, forming a four-membered Zn(2)O(2) ring.
