Trigonelline hydrochloride: A promising inhibitor for type I collagen fibrillation

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.