Curcumin Prevents the Glycation of Tricarboxylic Acid Cycle and Cell Respiration Proteins in the Heart of Mice Fed with a High-fructose Diet

Abstract

Background: A high fructose diet (HFD) induces protein glycation. The latter is related to a higher risk of cardiovascular disease. Curcumin is a natural pleiotropic compound that may possess antiglycant properties. Objective: To analyze the effect of curcumin on the content of glycated proteins in the hearts of 6-week-old mice fed with a HFD for 15 weeks. Methods: Mice were allocated in four groups (n = 6/group): a control group that received a standard diet (CT); a group that received 30% w/v fructose in water (F); a group that received 0.75% w/w curcumin supplemented in food (C); a group that received 30% w/v fructose in water and 0.75% w/w curcumin supplemented in food (F+C). The content of glycated proteins in the heart was determined by Western Blot (whereas the spots were detected by 2D-PAGE) using anti-AGE and anti-CML antibodies. A densitometric analysis was performed using the ImageLab software. Glycated proteins were identified by MALDI-TOF-MS, and an ontological analysis was performed in terms of biological processes and molecular function based on the STRING and DAVID databases. Results: Fourteen glycated protein spots were detected, two of them with anti-AGE and the other 12 with anti-CML. In total, eleven glycated proteins were identified, out of which three had decreased glycation levels due to curcumin exposure. The identified proteins participate in processes such as cellular respiration, oxidative phosphorylation, lipid metabolism, carbohydrate metabolism, the tricarboxylic acid cycle (TAC), and the organization of intermediate filaments. Conclusions: Curcumin decreased the fructose-induced glycation level of the ACO2, NDUFS7, and DLAT proteins.

Curcumin Sensitises Cancerous Kidney Cells to TRAIL Induced Apoptosis via Let-7C Mediated Deregulation of Cell Cycle Proteins and Cellular Metabolism

“…We previously reported that curcumin induced a redox imbalance by increasing ROS production and activation of the mitochondrial pathway of apoptosis thus sensitising ACHN cells to TRAIL induced death [16]. Similarly, other studies found that curcumin activated the TCA cycle [91,92] while reducing glucose consumption and lactate production. Curcumin can also induce reprogramming of tumour metabolism via targeting the ATP machinery of mitochondria, leading to the activation of apoptosis due to energy shutdown [93].…”