364 research outputs found
Inhibitory Activities of Cyanidin and Its Glycosides and Synergistic Effect with Acarbose against Intestinal α-Glucosidase and Pancreatic α-Amylase
Cyanidin and its glycosides are naturally dietary pigments which have been indicated as promising candidates to have potential benefits to humans, especially in the prevention and treatment of diabetes mellitus. We investigated the structure activity relationships of cyanidin and its glycosides to inhibit intestinal α-glucosidases and pancreatic α-amylase in vitro. The results found that cyanidin and its glycosides are more specific inhibitors of intestinal sucrase than intestinal maltase. Cyanidin-3-galactoside and cyanidin-3-glucoside were the most potent inhibitors against intestinal sucrase and pancreatic α-amylase with IC50 values of 0.50 ± 0.05 and 0.30 ± 0.01 mM, respectively. Our findings indicate that the structural difference between glucose and galactose at the 3-O-position of cyanidin was an important factor for modulating the inhibition of intestinal sucrase and pancreatic α-amylase. The combination of cyandin-3-glucoside, cyanidin-3- galactoside or cyanidin-3,5-diglucosides with a low concentration of acarbose showed synergistic inhibition on intestinal maltase and sucrase. The synergistic inhibition was also found for a combination of cyanidin or cyanidin-3-glucoside with a low concentration of acarbose. The findings could provide a new insight into a use for the naturally occurring intestinal α-glucosidase and pancreatic α-amylase inhibitors for the prevention and treatment of diabetes and its complications
The protective effects of pomelo extract (Citrus grandis L. Osbeck) against fructose-mediated protein oxidation and glycation
Chronic hyperglycemia induces non-enzymatic protein glycation, which plays an important
role in the development of diabetic complications. Immense efforts have been made to determine effective antiglycation compounds from natural products. Pomelo has shown beneficial effects for human health.
The objective of this study was to determine the antiglycation effect of pomelo extract against fructose-mediated protein oxidation and glycation. Our results showed that the pomelo extract (0.25 - 2.00 mg/mL) significantly inhibited the overall formation of advanced glycation end products (AGEs) in a concentration-dependent manner. The pomelo extract markedly decreased the level of fructosamine, which is directly associated with reduction in formation of AGEs and Nε -(carboxymethyl)lysine (CML). In addition, the pomelo extract inhibited protein oxidation through its ability to prevent the loss of thiol groups and reduced protein carbonyl formation. We characterized the active components in the pomelo extract by using high-performance liquid chromatography (HPLC), which showed that the pomelo extract contained naringin (11.90 ± 0.21 mg/g dried extract), hesperidin (12.04 ± 0.12 mg/g dried extract), neohesperidin (25.4 ± 0.12 mg/g dried extract), and naringenin (9.20 ± 0.19 mg/g dried extract). Our findings could provide a new insight into the antiglycation properties of the extract of the naturally occurring fruit pomelo for preventing AGE-mediated diabetic complications
Inhibitory effect of Clitoria ternatea flower petal extract on fructose-induced protein glycation and oxidation-dependent damages to albumin in vitro
Background: The accumulation of advanced glycation end products (AGEs) in body tissue has been implicated in the progression of age-related diseases. Inhibition of AGE formation is the imperative approach for alleviating diabetic complications. Clitoria ternatea extract (CTE) has been demonstrated to possess anti-diabetic activity. However, there is no scientific evidence supporting its anti-glycation activity. The objective of this study was to determine the inhibitory effect of CTE on fructose-induced formation of AGEs and protein oxidation. Antioxidant activity of CTE was also assessed by various methods. Methods: The aqueous extract of CTE (0.25-1.00 mg/ml) was measured for the content of total phenolic compounds, flavonoid, and anthocyanin by Folin-Ciocalteu assay, AlCl3 colorimetric method, and pH differential method, respectively. The various concentrations of CTE were incubated with BSA and fructose at 37 degrees C for 28 days. The formation of fluorescent AGEs, the level of fructosamine, protein carbonyl content, and thiol group were measured. The in vitro antioxidant activity was measured by the 1,1-diphenyl 2-picrylhydrazyl (DPPH) scavenging activity, trolox equivalent antioxidant capacity (TEAC), ferric reducing antioxidant power (FRAP), hydroxyl radical scavenging activity (HRSA), superoxide radical scavenging activity (SRSA), and ferrous ion chelating power (FICP). Results: The results demonstrated that the content of total phenolics, flavonoids and total anthocyanins in CTE was 53 +/- 0.34 mg gallic acid equivalents/g dried extract, 11.2 +/- 0.33 mg catechin equivalents/g dried extract, and 1.46 +/- 0.04 mg cyanidin-3-glucoside equivalents/g dried extract, respectively. Moreover, CTE (0.25-1.00 mg/ml) significantly inhibited the formation of AGEs in a concentration-dependent manner. CTE also markedly reduced the levels of fructosamine and the oxidation of protein by decreasing protein carbonyl content and preventing free thiol depletion. In the DPPH radical scavenging activity and SRSA, CTE had the IC50 values of 0.47 +/- 0.01 mg/ml and 0.58 +/- 0.04 mg/ml. Furthermore, the FRAP and TEAC values of CTE were 0.38 +/- 0.01 mmol FeSO4 equivalents/mg dried extract and 0.17 +/- 0.01 mg trolox equivalents/mg dried extract. However, CTE showed weak scavenging activity on hydroxyl radical and a weak antioxidant iron chelator. Conclusions: The results showed that CTE has strong antiglycation and antioxidant properties and might have therapeutic potentials in the prevention of AGE-mediated diabetic complications
Cyanidin-3-rutinoside alleviates postprandial hyperglycemia and its synergism with acarbose by inhibition of intestinal α-glucosidase
The inhibitory activity on intestinal α-glucosidase by cyanidin-3-rutinoside was examined in vitro and in vivo. The IC50 values of cyanidin-3-rutinoside against intestinal maltase, and sucrase were 2,323 ± 14.8 and 250.2 ± 8.1 µM, respectively. The kinetic analysis revealed that intestinal sucrase was inhibited by cyanidin-3-rutinoside in a mixed-type manner. The synergistic inhibition also found in combination of cyanidin-3-rutinoside with acarbose against intestinal maltase and sucrase. The oral administration of cyanidin-3-rutinoside (100 and 300 mg/kg) plus maltose or sucrose to normal rats, postprandial plasma glucose was markedly suppressed at 30–90 min after loading. Furthermore, the normal rats treated with acarbose and cyanidin-3-rutinoside (30 mg/kg) showed greater reduction of postprandial plasma glucose than the group treated with acarbose alone. These results suggest that cyanidin-3-rutinoside retards absorption of carbohydrates by inhibition of α-glucosidase which may be useful as a potential inhibitor for prevention and treatment of diabetes mellitus
Cinnamic Acid and Its Derivatives Inhibit Fructose-Mediated Protein Glycation
Cinnamic acid and its derivatives have shown a variety of pharmacologic properties. However, little is known about the antiglycation properties of cinnamic acid and its derivatives. The present study sought to characterize the protein glycation inhibitory activity of cinnamic acid and its derivatives in a bovine serum albumin (BSA)/fructose system. The results demonstrated that cinnamic acid and its derivatives significantly inhibited the formation of advanced glycation end products (AGEs) by approximately 11.96–63.36% at a concentration of 1 mM. The strongest inhibitory activity against the formation of AGEs was shown by cinnamic acid. Furthermore, cinnamic acid and its derivatives reduced the level of fructosamine, the formation of Nɛ-(carboxymethyl) lysine (CML), and the level of amyloid cross β-structure. Cinnamic acid and its derivatives also prevented oxidative protein damages, including effects on protein carbonyl formation and thiol oxidation of BSA. Our findings may lead to the possibility of using cinnamic acid and its derivatives for preventing AGE-mediated diabetic complications
The Alterations of Erythrocyte Phospholipids in Type 2 Diabetes Observed after Oral High-Fat Meal Loading: The FTIR Spectroscopic and Mass Spectrometric Studies
Little is known about the postprandial remodelling of erythrocytes phospholipids (PLs) in type 2 diabetics (T2DM). Therefore, this study aims to compare the alterations of erythrocyte PLs in T2DM to those of healthy subjects after ingestion of a high-fat meal. Eleven T2DM and ten healthy subjects underwent a high-fat meal loading. Erythrocytes were isolated from blood obtained after fasting and 4 h after the meal. Fourier Transform Infrared (FTIR) spectroscopy was initially used to screen erythrocyte PLs by monitoring C-H stretching vibrations. Phosphatidylcholine (PC) molecular species were further investigated by Liquid Chromatography-Electrospray Ionisation-Mass Spectrometry (LC-ESI-MS). For the control group, FTIR revealed postprandial changes in C-H stretching vibrations, particularly of the olefinic band. These findings were supported by LC-ESI-MS data, showing marked changes in PC molecular species, especially of the PC34:1 (where 34 and 1 mean the summed number of carbons and double bonds, respectively). However, similar changes of those were not apparent in the T2DM group. Our results reveal marked postprandial alterations of erythrocyte PC species in healthy subjects whereas only mild alterations are observed in T2DM. The discrepant effects of high-fat meal loading suggest abnormal PC remodelling in the diabetic erythrocyte that may affect its membrane fluidity and integrity
The effect of mimicking febrile temperature and drug stress on malarial development
<p>Abstract</p> <p>Background</p> <p>Malaria remains one of the most important tropical diseases of human with 1–2 million deaths annually especially caused by <it>P. falciparum</it>. During malarial life cycle, they exposed to many environmentally stresses including wide temperature fluctuation and pharmacological active molecules. These trigger malarial evolutionarily adaptive responses. The effect of febrile temperature on malarial growth, development and drug susceptibility by mimicking patient in treatment failure before and after drug uptake was examined.</p> <p>Methods</p> <p>Sensitivities of <it>P. falciparum </it>to antimalarial drug (chloroquine, mefloquine, quinine and artesunate) were investigated based on the incorporation of [<sup>3</sup>H] hypoxanthine into parasite nucleic acids or radioisotopic technique. The number of parasites was examined under microscope following Giemsa staining and the parasite development at the end of each phase was counted and comparison of parasite number was made. The proteome was separated, blotted and hybridized with anti-Hsp70s primary antibody. The hybridized proteins were separately digested with trypsin and identified by MALDI-TOF peptide mass fingerprint.</p> <p>Results</p> <p>The results show that febrile temperature is capable of markedly inhibiting the growth of field isolate <it>P. falciparum </it>but not to K1 and 3D7 standard strains. K1 and 3D7 grown under heat shock developed greater and the reinfection rate was increased up to 2-folds when compared to that of non-heat shock group. The IC<sub>50 </sub>value of K1 toward chloroquine, mefloquine and quinine under heat shock was higher than that of K1 under non-heat shock which is opposite to that of 3D7. Heat shock caused death in field isolated parasite. It was also found that the febrile temperature coped with chloroquine uptake had no effect to the development, drug sensitivity and the parasite number of K1 strain. In the opposite way, heat shock and chloroquine shows extremely effect toward 3D7 and field isolate PF91 as shown by higher number of dead parasites compared to that of control group. After culture under high temperature with artesunate, the total parasite number of all strains including K1, 3D7 and PF91 was extremely decreased and the parasite was not found at the end. Additionally, the expression of <it>pf</it>Hsp70s was found in all strains and conditions as shown in 120 kDa hybridized band. However, the proteome extracted from K1 grown under heat shock with chloroquine, anti-<it>pf</it>Hsp70 interacted with additional three bands identified by MALDI-TOF as elongation factor-1α (83 kDa), pf<it>Hsp</it>86 (60 kDa) and phosphoethanolamine <it>N</it>-methyltransferase (43 kDa).</p> <p>Conclusion</p> <p>In conclusion, febrile temperature was capable of markedly inhibiting the growth of field isolate <it>P. falciparum </it>while the development, reinfection rate and drug (chloroquine, mefloquine and quinine) resistant level of standard strain K1 was enhanced. However, the febrile temperature coped with chloroquine had no effect to the development, drug sensitivity and the parasite number of K1 strain. In the opposite way, heat shock and chloroquine showed extremely effect toward 3D7 and field isolate PF91 as shown by some died parasites. Heat shock protein 70 (<it>pf</it>HSP70) of strain K1 under heat shock with chloroquine might involved in many pathways in order to sustain the parasite.</p
Clitoria ternatea Flower Petal Extract Inhibits Adipogenesis and Lipid Accumulation in 3T3-L1 Preadipocytes by Downregulating Adipogenic Gene Expression
Clitoria ternatea (commonly known as blue pea) flower petal extract (CTE) is used as a natural colorant in a variety of foods and beverages. The objective of study was to determine the inhibitory effect of CTE on adipogenesis in 3T3-L1 preadipocytes. The phytochemical profiles of CTE were analyzed by liquid chromatography and tandem mass spectrometry (LC-MS/MS). Anti-adipogenesis effect of CTE was measured by using Oil Red O staining, intracellular triglyceride assay, quantitative real-time PCR and western blot analysis in 3T3-L1 adipocytes. Cell cycle studies were performed by flow cytometry. Lipolysis experiments were performed using a colorimetric assay kit. In early stages, CTE demonstrated anti-adipogenic effects through inhibition of proliferation and cell cycle retardation by suppressing expression of phospho-Akt and phospho-ERK1/2 signaling pathway. The results also showed that CTE inhibited the late stage of differentiation through diminishing expression of adipogenic transcription factors including PPARγ and C/EBPα. The inhibitory action was subsequently attenuated in downregulation of fatty acid synthase and acetyl-CoA carboxylase, causing the reduction of TG accumulation. In addition, CTE also enhanced catecholamine-induced lipolysis in adipocytes. These results suggest that CTE effectively attenuates adipogenesis by controlling cell cycle progression and downregulating adipogenic gene expression
Interaction between ascorbic acid and gallic acid in a model of fructose-mediated protein glycation and oxidation
Background: Dietary plant-based foods contain combinations of various
bioactive compounds such as phytochemical compounds and vitamins. The
combined effect of these vitamins and phytochemicals remains unknown,
especially in the prevention of diabetes and its complications. The
present study aimed to investigate the combined effect of ascorbic acid
and gallic acid on fructose-induced protein glycation and oxidation.
Results: Ascorbic acid (15 \u3bcg/mL) and gallic acid (0.1 \u3bcg/mL)
reduced fructose-induced formation of advanced glycation end products
(AGEs) in bovine serum albumin (BSA; 10 mg/mL) by 15.06% and 37.83%,
respectively. The combination of ascorbic acid and gallic acid
demonstrated additive inhibition on the formation of AGEs after 2 weeks
of incubation. In addition, synergistic inhibition on the formation of
amyloid cross-\u3b2 structure and protein carbonyl content in
fructose-glycated BSA was observed. At the same concentration, the
combination of ascorbic acid and gallic acid produced a significant
additive effect on the 2,2-diphenyl-1-picrylhydrazyl radical scavenging
activity. Conclusion: Combining natural compounds such as ascorbic acid
and gallic acid seems to be a promising strategy to prevent the
formation of AGEs
Real-Time PCR Detection and Phylogenetic Relationships of \u3ci\u3eNeorickettsia\u3c/i\u3e In Digeneans From Egypt, Phillipines, Thailand, Vietnam and the United States
Neorickettsia (Rickettsiales, Anaplasmataceae) is a genus of obligate intracellular bacterial endosymbionts of digeneans (Platyhelminthes, Digenea). Some Neorickettsia are able to invade cells of the digenean\u27s vertebrate host and are known to cause diseases of domestic animals, wildlife, and humans. In this study we report the results of screening digenean samples for Neorickettsia collected from bats in Egypt and Mindoro Island, Philippines, snails and fishes from Thailand, and fishes from Vietnam and the USA. Neorickettsia were detected using a real-time PCR protocol targeting a 152bp fragment of the heat shock protein coding gene, GroEL, and verified with nested PCR and sequencing of a 1853bp long region of the GroESL operon and a 1371bp long region of 16S rRNA. Eight unique genotypes of Neorickettsia were obtained from digenean samples. Neorickettsia sp. 8 obtained from Lecithodendrium sp. from Egypt; Neorickettsia sp. 9 and 10 obtained from two species of Paralecithodendrium from Mindoro, Philippines; Neorickettsia sp. 11 from Lecithodendrium sp. and Neorickettsia sp. 4 (previously identified from Saccocoelioides lizae, from China) from Thailand; Neorickettsia sp. 12 from Dicrogaster sp. Florida, USA; Neorickettsia sp. 13 and SF agent from Vietnam. Sequence comparison and phylogenetic analysis demonstrated that the forms, provisionally named Neorickettsia sp. 8-13, represent new genotypes. We have for the first time detected Neorickettsia in a digenean from Egypt (and the African continent as a whole), the Philippines, Thailand and Vietnam based on PCR and sequencing evidence. Our findings suggest that further surveys from the African continent, SE Asia, and island countries are likely to reveal new Neorickettsia lineages as well as new digenean host associations
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