The
structure and in vitro antiproliferative activity
of anthocyanins in the root tubers of a sweet potato variety cv. Bhu
Krishna and the purple leaves of a promising accession S-1467 were
studied with the objectives of understanding the structure–activity
relationship and comparing the leaf and tuber anthocyanins. The chemical
structure of anthocyanins was determined by high-resolution electrospray
ionization mass spectrometry analysis. A fluorescence-resonance-energy-transfer-based
caspase sensor probe had been used to study the antiproliferative
property, and analysis of the cell cycle was performed after staining
with propidium iodide and subsequent fluorescence-activated cell sorting.
Structurally, the anthocyanins in root tubers were identical to those
in leaves, but there was a difference in the proportion of various
aglycones present in both. This has led to distinguishable differences
in the antiproliferative activity of leaf and tuber anthocyanins to
various cancer cells. All nine anthocyanins were found in acylated
forms in both tubers and leaves. However, peonidin derivatives were
major anthocyanins in tubers (33.98 ± 1.41 mg) as well as leaves
(27.68 ± 1.07 mg). The cyanidin derivatives were comparatively
higher in leaves (20.55 ± 0.91 mg) than tubers (9.44 ± 0.94
mg). The tuber and leaf anthocyanins exhibited potential antiproliferative
properties to MCF-7, HCT-116, and HeLa cancer cells, and the structure
of anthocyanins had a critical role in it. The leaf anthocyanins exhibited
significantly higher activity against colon and cervical cancer cells,
whereas tuber anthocyanins had a slightly greater effect against breast
cancer cells.
Objectives:This study was planned to investigate the effects of pre and post-treatment of young inflorescence of Cocos nucifera (CnI) on alloxan-induced diabetic rats.Materials and Methods:Male albino Sprague Dawely rats were divided into five groups of six animals each. Group I was normal control, Group II was diabetic control, Cocos nucifera Inflorescence (CnI) was fed along with diet [20% (w/w)] orally (Group III) for a period of 11 days prior to alloxan injection (150 mg/kg i.p.). The curative effect of CnI was evaluated at the same feeding levels in alloxan-induced diabetic rats (Group IV) for a period of 30 days. The effects of both pretreatment and post-treatment (Group V) were also evaluated. Biochemical parameters such serum glucose, hepatic glycogen, and enzymes involving carbohydrate metabolism (hexokinase, phosphoglucomutase, pyruvate kinase, glucose-6-phosphatase, fructose 1, 6-diphosphatase, glucose-6 phosphate dehydrogenase, and glycogen phosphorylase) were assayed along with pancreatic histopathology. Data were analyzed using one-way analysis of variance followed by Duncan's post hoc multiple variance test. P < 0.05 was considered statistical significant.Results:Diabetic control rats showed significant increase in serum glucose (P < 0.05) and decrease in hepatic glycogen levels (P < 0.05) compared to normal rats, which was reversed to near normal in both CnI pretreated and post-treated rats. Treatment with CnI resulted in significant decrease (P < 0.05) in activities of gluconeogenic enzymes in Group III and IV on compared to the diabetic control group, while glycolytic enzyme activities were improved in these groups. The cytotoxicity of pancreatic islets also ameliorated by treatment with CnI on histopathological examination.Conclusion:The results obtained in the study indicate the protective and curative effects of CnI on alloxan-induced pancreatic cytotoxicity, which is mediated through the regulation of carbohydrate metabolic enzyme activities and islets cell repair.
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