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Trigonelline hydrochloride: A promising inhibitor for type I collagen fibrillation

[Display omitted] •Implication drawn from this study, is an effective inhibition of type I collagen fibrillation by trigonelline hydrochloride.•Reduction in fibril diameter and packing density, suggesting an increase in electrostatic repulsion.•Compactness of structural-functional relationship and f...

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Published in:Colloids and surfaces, B, Biointerfaces B, Biointerfaces, 2018-10, Vol.170, p.273-279
Main Authors: Rasheeda, K., Fathima, N. Nishad
Format: Article
Language:English
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Summary:[Display omitted] •Implication drawn from this study, is an effective inhibition of type I collagen fibrillation by trigonelline hydrochloride.•Reduction in fibril diameter and packing density, suggesting an increase in electrostatic repulsion.•Compactness of structural-functional relationship and fibril formation of collagen at interfibrillar level.•Trigonelline hydrochloride is a potential candidate for targeted treatment of collagen accumulation pathologies. Collagen is a major structural protein, with properties such as low toxicity, low immune response and promoting cellular growth. If there is an excess of collagen accumulation, especially in the myocardium it leads to fibrosis, which in turn impairs the normal functioning of the myocardial tissues. In order to overcome collagen fibrillation, trigonelline hydrochloride has been used in this study as a potential agent for inhibiting the spontaneous self-assembly of type I collagen. Trigonelline hydrochloride, a nicotinic acid derivative is largely found in Trigonella foenum-graecum L. (fenugreek). Experimental work on turbidity assay shows that there is an increase in the lag phase compared to the native collagen indicating a delay in fibrillation. According to rheological aspects, viscosity of the collagen composite decreases due to the increase in shear rate, which disentangles the aggregated particles of collagen fibrils and allows it to align along the direction of rate. Morphological assessments through AFM and HR-SEM suggest that there is an effective reduction in fibrillation with an increase in the concentration of trigonelline hydrochloride. FT-IR (ATR) studies indicate that compactness of secondary structure helicity occurs on treatment with trigonelline hydrochloride. Such promising effect of trigonelline on collagen fibrillogenesis can be judiciously used for targeting specific sites of collagen accumulation via innovative drug delivery systems.
ISSN:0927-7765
1873-4367
DOI:10.1016/j.colsurfb.2018.06.030