Apigenin and quercetin ameliorate mitochondrial alterations by tunicamycin-induced ER stress in 3T3-L1 adipocytes.

Endoplasmic reticulum (ER) is an important organelle with functions like protein synthesis, folding, and calcium homeostasis. ER stress, a condition that dramatically affects protein folding homeostasis in cells, has been associated with a number of metabolic disorders. Emerging clinical and preclinical evidence support the notion that pharmacological modulators of ER stress have therapeutic potential as a novel target for treating metabolic diseases. ER is in physical contact with mitochondria, and there is a strong cross talk between these organelles at functional level. The present investigation was aimed to check the mitochondrial alterations in adipocytes with tunicamycin-induced ER stress and modulation by apigenin and quercetin. For this, differentiated adipocytes were incubated with tunicamycin (2 μg/ml) for 18 h, and changes in mitochondrial membrane potential, biogenesis, reactive oxygen species production, and adiponectin secretion were seen. Tunicamycin-induced ER stress altered reactive oxygen species (ROS) (6.34-fold↑), membrane potential (4.1-fold↑), mitochondrial biogenesis (2.4-fold↓), and adiponectin secretion (3.5-fold↓). Apigenin and quercetin ameliorated alterations in mitochondria. From results, we conclude that ER stress significantly alters mitochondrial functions and both the bioactives significantly protected mitochondrial alterations during ER stressand reestablished adiponectin secretion.