The analysis of coffee-green tea-turmeric combination against cardiac-metabolic syndrome using metabolite profiling, gene expression, and in silico approach

Author:

Rachmawati ErminORCID,Rohman Mohammad S.ORCID,Widodo NashiORCID,Lukitasari MifetikaORCID,Nugroho Dwi A.ORCID,Hermanto Feri E.ORCID,Kholis Mukhamad N.ORCID

Abstract

Context: The development of functional drinks to inhibit oxidative stress and inflammation as a critical process in inducing heart damage in metabolic syndrome is required. Coffee, tea, and turmeric have all been shown to offer health advantages. Aims: To investigate the effect of coffee, green tea, turmeric extract (ECGTT) against cardiac-metabolic syndrome (MetS). Methods: The secondary metabolites from coffee, green tea, and turmeric were identified using LC-HRMS. Male Sprague–Dawley rats were divided into four groups (n = 4) representing normal, MetS, MetS with ECGTT treatment doses: 300/100/150 mg/BW and 300/100/250 mg/BW group. Upon the end of treatment periods, expression of tumor necrosis factor-alpha (TNFα), interleukin-6 (IL-6), nuclear factor kappa B (NF-κB), NADPH oxidase (NOX2), SERCA2a were measured from the heart. A computational approach including network pharmacology, protein-protein interaction (PPI) network, molecular docking, and dynamic was performed to understand the molecular mechanism of ECGTT against cardiac damage in MetS. Results: Chlorogenic acid (CGA), epigallocatechin gallate (EGCG), and curcumin were identified as the main metabolites in ECGTT. The ECGTT administration decreased the TNFα, IL-6, NF-κB, and NOX2 and increased SERCA2a expression(p<0.05). Moreover, the PPI result suggested that angiotensin II receptor type 1 (AGTR1) was the key regulator of cardiac injury-MetS induced. CGA, EGCG, and curcumin bind to AGTR1 with smaller binding energy than metformin and showed stability of structure and interaction among those metabolites into AGTR1. Conclusions: Coffee, green tea, and turmeric might prevent heart dysfunction in MetS through modulation of oxidative stress and inflammation.

Publisher

Garval Editorial Ltda.

Subject

Drug Discovery,Pharmaceutical Science,Pharmacology,Pharmacy,Complementary and alternative medicine

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