Prevention of Protein Glycation by Natural Compounds
Abstract
:1. Glycation
2. Glycation and Ageing
3. Inhibition of Glycation
4. Inhibition of Glycation in Vitro
5. Inhibition of Glycation in Vivo
5.1. Reduction of AGE Intake
5.2. Effect of Exogenous Compounds of Natural Origin
5.2.1. Problems with Exogenous Modification of Glycation
5.2.2. Effects of Natural Compounds
5.2.3. Effects of AGE Breakers
Population | Intervention | Main Findings | Reference |
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Healthy male Sprague–Dawley rats (220 ± 20 g) were divided randomly into four groups each containing 10 rats: control group, fructose group, betanin 25 mg/kg per day group, and betanin 100 mg/kg per day group. | Fructose water solution (30%) was accessed freely, and betanin (betanidin 5-O-β-d-glucoside, red) (25 and 100 mg/kg/d) was administered by intra-gastric gavage continuously for 60 days. | Betanin decreased protein glycation indexed by the relative lower methylglyoxal/ N-carboxymethyl lysine (CML) level and RAGE expression, and reduced glycative products in BSA/fructose system. Betanin also antagonized oxidative stress and NF-κB activation, all of them may be involved in the antifibrotic mechanisms. Food pigments may neutralize adverse effects of carbohydrate, i.e., diabetes and related syndrome, and complementary therapy with betanin may prove useful in attenuating the development of cardiac fibrosis in diabetes. | [116] |
Male C57 BLKS/J genetic background (db/db) mice and their non-diabetic lean littermates (db/m; 6-wk-old)were randomly divided into five groups (n = 8 each). | Mice were orally administered vehicle (sterile distilled water), metformin (300 mg/kg), and (+)-catechin (15, 30, and 60 mg/kg fresh preparation with sterile distilled water) daily at 4:00 pm, continuously for 16 weeks. Metformin was used as a positive antidiabetic drug, and db/m mice were used as non-diabetic controls. After 4–6 h fasting at the end of the treatment period, mice were killed and kidney tissues were saved for further assays. | (+)-Catechin might ameliorate renal dysfunction in diabetic mice as consequences of inhibiting AGEs formation and cutting off inflammatory pathway via methylglyoxal trapping. | [117] |
Two-month-old male Wistar NIN rats with an average bodyweight of 220 ± 17 g were used in the study. Animals were distributed into four groups (groups I–IV). Each group consists of six animals. | All the animals were fed with AIN-93 diet ad libitum. The control (group I) rats received sham consists of 0.1 M citrate buffer, pH 4.5 while the experimental rats received a single i.p injection of streptozotocin (STZ, 35 mg/kg) in citrate buffer. Animals in group II received AIN-93 diet alone whereas group III animals received the AIN-93 diet supplemented with 3% cinnamon powder whereas group IV animals received AIN-93 diet containing 0.002% procyanidin-B2 -fraction. All the animals had free access to water. | Supplementation of diabetic rats with cinnamon and procyanidin-B2 -fraction prevented glycation mediated RBC-IgG cross-links and HbA1c accumulation in diabetes rats. Cinnamon and procyanidin-B2 -fraction also inhibited the accumulation of CML, a prominent AGE in diabetic kidney. Cinnamon and its procyanidin-B2 -fraction prevented the AGE mediated loss of expression of glomerular podocyte proteins; nephrin and podocin. Inhibition of AGE by cinnamon and procyanidin-B2 -fraction ameliorated the diabetes mediated renal malfunction in rats as evidenced by reduced urinary albumin and creatinine. Procyanidin-B2 from cinnamon inhibited AGE accumulation in diabetic rat kidney and ameliorated AGE mediated pathogenesis of diabetic nephropathy. | [118] |
Male Wistar rats (200–230 g) were obtained from Sanzyme Ltd. (Hyderabad, India). The animals were divided into 4 groups (n = 8). | Diabetes was induced in all the male Wistar rats (200–250 g) except a group of eight animals which were treated as naïve (group I) by intraperitoneal administration of STZ (45 mg/kg) dissolved in freshly prepared citrate buffer (pH 4.5). The animals were fasted for 12 h before STZ administration and supplemented with 10% glucose for 48 h after STZ administration. One week after streptozotocin administration, blood glucose was estimated and the animals with more than 300 mg/dL were treated as diabetic and after a period of 6 weeks, the animals were divided into 3 groups. Group II served as diabetic control where as group III and group IV received resveratrol (10 mg/kg) and fidarestat (1 mg/kg), by per oral administration respectively, for a period of 3 weeks. | Resveratrol significantly improved glycaemic status and renal function in diabetic rats with a significant decrease in the formation of AGEs in the kidneys. | [119] |
Male Wistar rats (initial weight of 50–75 g) were obtained from Charles River Breeding Laboratories (St-Constant, Qc, Canada). The animals were divided into six groups (Ctr3, n = 10; D3, n = 8; PYR, n = 8; Ctrl7, n = 9; D7, n = 8; ALA, n = 7). | Rats were fed a high fat diet containing rodent diet D12451 (45 kcal % fat, 35 kcal % carbohydrates and 20 kcal % protein; Research Diets, New Brunswick, NJ, USA) ad libitum during 8 weeks, followed by a single dose of STZ (30 mg/kg intra-peritoneally). Four weeks after the injection of STZ, rats received warfarin (20 mg kg−1 day−1 in drinking water) and vitamin K (phylloquinone, 15 mg kg−1 day−1 sub-cutaneous injection, Spectrum Chemical, New Brunswick, NJ, USA) during 3 (D3), 5 (D5) and 7 (D7) weeks. To determine the implication of AGEs in initiating elasto-calcinosis, a subgroup of D3 rats received pyridoxamine (200 mg. kg−1 day−1) in powdered chow starting the same day as the STZ injection (thus during 7 weeks, including the 3 weeks of warfarin vitamin K (WVK) treatment) to prevent AGEs formation (group labeled PYR). To study the role of AGEs later in the calcification process, alagebrium (10 mg. kg−1 day−1, Synvista, Montvale, NJ, USA) was introduced in the food 7 weeks after the STZ injection (after 3 weeks of WVK treatment) and rats studied 4 weeks later (group labeled ALA). Dosages were adjusted every second day according to food intake. Controls consisted of age-matched untreated rats (Ctrl3 or Ctrl7). | Pyridoxamine (PYR) prevented AGE accumulation, whereas alagebrium chloride (ALT-711) induced a regression of AGE cross-links. PYR prevented calcium accumulation, while alagebrium blunted the progression of calcification. | [120] |
Sprague Dawley (SD) rats were divided into five groups (n = 9 each). | Diabetes was induced by a single injection of streptozotocin (STZ, 60 mg/kg, intraperitoneally) in rats. Age-matched control rats (aged 6 weeks) received an equal volume of vehicle (0.01 M citrate buffer, pH 4.5). To investigate the effects of Cassiae semen (CS) extract, treatment was begun one week after the onset of diabetes and the compound was orally administered to the rats once a day for 12 weeks. SD rats were divided into groups: (1) normal rats (N), (2) normal rats treated with CS (N + CS), (3) STZ-induced diabetic rats (DM), (4) STZ-induced diabetic rats treated with CS (DM + CS, 100 mg/kg body weight), and (5) STZ-induced diabetic rats treated with aminoguanidine (AG), a positive control for AGEs inhibitor (DM + AG, 100 mg/kg body weight). | Oral treatment of CS can inhibit the development of diabetic nephropathy via inhibition of AGEs accumulation in STZ-induced diabetic rats The CS-treated group had significantly inhibited COX-2 mRNA and protein, which mediates the symptoms of inflammation in the renal cortex of diabetic rats. Histopathological studies of kidney tissue showed that in diabetic rats, AGEs, the receptor for AGEs, TGF-β1, and collagen IV were suppressed by CS treatment. | [121] |
In vivo experiments were performed on 6-week-old male Wistar albino rats weighing 180–200 g. The animals were divided into 12 groups, each containing six animals, and each test sample was given to two groups of rats. | The control and all test groups were orally fed with galactose at a dose of 10 mg/kg body weight. Boswellic acid, corsolic acid, ellagic acid ursolic acid and quercetin were given at a dose of 10 mg/kg body weight. All the animals were sacrificed on the 15th day by spinal nerve dislocation. | All the tested extracts and their active ingredients possess significant the polyol enzyme aldose reductase inhibitory actions with urosolic acid showing the most potent effect. The study indicates the potential of the studied plants and their major constituents as possible protective agents against long-term diabetic complications. | [122] |
A total of 48 male Kunming mice were used (four groups, 12 mice in each group). | The aggregated Aβ25–35 was injected into the right lateral ventricle with the following coordinates: −0.5 mm anterior/posterior, +1.0 mm medial/lateral and −2.5 mm dorsal/ventral from Bregma (10 nmol in 3 μL of saline per injection). Sham animals were injected in an identical manner with the same amount of sterile saline. Mice were allocated to one of four groups the day after sterile saline or Aβ25–35 injection: sham group, Aβ25–35-treated group, pinocembrin 20 mg/kg group, and pinocembrin 40 mg/kg group. Pinocembrin was administered by oral gavage once a day continuously for 8 days. The sham group and Aβ25–35-treated group received oral gavage in the same manner using distilled water containing 20% hydroxypropyl-β-cyclodextrin without pinocembrin. | Pinocembrin (a flavonoid abundant in propolis), significantly inhibited the upregulation of RAGE transcripts and protein expression both in vivo and in vitro, and also markedly depressed the activation of p38 mitogen-activated protein kinase (MAPK)-MAPKAP kinase-2 (MK2)-heat shock protein 27 (HSP27) and stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK)-c-Jun pathways and the downstream nuclear factor κB (NFκB) inflammatory response subsequent to Aβ-RAGE interaction. Pinocembrin significantly alleviated mitochondrial dysfunction through improving mitochondrial membrane potential and inhibiting mitochondrial oxidative stress, and regulated mitochondrion-mediated apoptosis by restoration of B cell lymphoma 2 (Bcl-2) and cytochrome c and inactivation of caspase 3 and caspase 9. | [123] |
Zebrafish maintenance and experimental procedures were approved by the Committee of Animal Care and Use of Yeungnam University (Gyeongsan, South Korea). Each group (n = 70) consumed the designated diet (20 mg/day/fish). | A high cholesterol (HC) diet containing 4% cholesterol was made by soaking tetrabit [Tetrabit Gmbh D49304; 47.5% crude protein, 6.5% crude fat, 2.0% crude fiber, 10.5% crude ash, containing vitamin A (29,770 IU/kg), vitamin D3 (1860 IU/kg), vitamin E (200 mg/kg), and vitamin C (137 mg/kg); (Melle, Germany)] in a solution of cholesterol in diethyl ether. After ether evaporation, HC diet was mixed with lyophilized fruit extract (a final concentration of 10% w/w of powder/ tetrabit). The animals were divided into 5 groups: normal diet (ND) group, high cholesterol (HC) diet group, HC + LL (loquat leaves) group, acai-fed group (HC + acai) and HC + GS (grape skin) group. | Serum glucose levels increased in the high cholesterol diet group, to threefold above the ND group; GS and LL feeding elicited the greatest reduction in hyperglycemia. The groups consuming acai and LL showed much less hepatic inflammation, as well as attenuation of fatty liver and a reduced content of oxidized species. | [124] |
A total of 15 male inbred C57BL/6 J mice were used (3 groups, 5 mice in each group). | Diabetes was induced in the mice by a single dose of STZ (200 mg/kg). Mice were fed a normal rodent chow diet (Clea Japan) for 1 week after induction of diabetes. At this time, these mice were administered epicatechin (500 mg/kg/day) orally every day for 45 days. Animals were divided into groups: control group, mice treated with epicatechin (500 mg/kg/day), and mice treated with arbutin, a catechol analogue (500 mg/kg/day). | Administration of 500 mg/kg/day epicatechin to STZ-induced diabetic mice enhanced the CML accumulation on the surface of gastric epithelial cells, whereas administration of 500 mg/kg/day arbutin to STZ-induced diabetic mice did not enhance CML accumulation compared to untreated mice. High amounts of catechol-containing structures enhance oxidative stress, thus leading to enhanced CML formation, and this phenomenon may explain the paradoxical effect that some flavonoids have on redox status. | [111] |
Adult male Wistar rats of body weight 150–160 g were used in the study. The animals were divided into four groups of six rats each. | Control animals (CON) received the control diet containing starch and tap water ad libitum. Fructose-fed animals (FRU) received the high fructose diet and water ad libitum. Fructose-fed animals (FRU-CA) received the high fructose diet and water ad libitum and were administered 300 mg carnitine (CA)/kg b.w/day; i.p. Control animals (CON-CA) received the control diet and water ad libitum and were administered with 300 mg CA/kg b.w/day; i.p. | The levels of glucose, fructose and fructosamine in plasma and glycated haemoglobin and methyl glyoxal in blood were significantly higher in fructose-fed animals than in the control rats. Administration of CA along with the fructose diet reduced these levels significantly. In rats fed control diet, administration of CA did not produce significant alterations in the parameters when compared with the control group. The rats fed fructose diet showed increased total collagen and glycation in tail tendon and skin as compared to control rats. CA-administered fructose-fed rats registered near-normal levels of collagen and glycation. No significant changes were observed in control rats treated with CA. | [84] |
6. Conclusions
Acknowledgments
Author Contributions
Conflicts of Interest
References
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Sadowska-Bartosz, I.; Bartosz, G. Prevention of Protein Glycation by Natural Compounds. Molecules 2015, 20, 3309-3334. https://doi.org/10.3390/molecules20023309
Sadowska-Bartosz I, Bartosz G. Prevention of Protein Glycation by Natural Compounds. Molecules. 2015; 20(2):3309-3334. https://doi.org/10.3390/molecules20023309
Chicago/Turabian StyleSadowska-Bartosz, Izabela, and Grzegorz Bartosz. 2015. "Prevention of Protein Glycation by Natural Compounds" Molecules 20, no. 2: 3309-3334. https://doi.org/10.3390/molecules20023309