Mitochondrial connection to ginsenosides
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Online ISSN 1976-3786 Print ISSN 0253-6269
REVIEW
Mitochondrial connection to ginsenosides Feng Wang1 · Yoon Seok Roh1
Received: 19 August 2020 / Accepted: 22 October 2020 / Published online: 28 October 2020 © The Pharmaceutical Society of Korea 2020
Abstract Mitochondria play an essential role in energy synthesis and supply, thereby maintaining cellular function, survival, and energy homeostasis via mitochondria-mediated pathways, including apoptosis and mitophagy. Ginsenosides are responsible for most immunological and pharmacological activities of ginseng, a highly beneficial herb with antioxidant, anti-inflammatory, anti-apoptotic, and neuroprotective properties. Studies have shown that ginsenosides assist in regulating mitochondrial energy metabolism, oxidative stress, biosynthesis, apoptosis, mitophagy, and the status of membrane channels, establishing mitochondria as one of their most important targets. This article reviews the regulatory effects of ginsenosides on the mitochondria and highlights their beneficial role in treating mitochondrial diseases. Keywords Mitochondria · Ginsenosides · Energy metabolism · Oxidative stress · Apoptosis · Mitophagy
Introduction Mitochondria are organelles with outer and inner membranes composed of phospholipid bilayers and proteins that play a prominent role in energy production. A doublemembraned organization creates five distinct parts, including the outer mitochondrial membrane, intermembrane space (between the outer and inner membranes), the inner mitochondrial membrane, cristae space (formed by infolds of the * Yoon Seok Roh [email protected] 1
Department of Pharmacy, College of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju, Chungbuk 28160, South Korea
inner membrane), and matrix (space within the inner membrane). As organelles with their own DNA, mitochondria are involved in several metabolic processes of eukaryotic cells, including energy conversion, pyruvate metabolism and the citric acid cycle, Nicotinamide adenine dinucleotide (NADH) and Flavin adenine dinucleotide (FADH2) production in the electron transport chain, thermogenesis, storage of calcium ions, and apoptosis (programmed cell death). The primary functions of the mitochondria are to produce the energy currency of the cell, Adenosine triphosphate (ATP), via respiration, and to regulate cellular metabolism (Schmidt-Rohr 2020). Mitochondrial damage and subsequent dysfunction are important factors in several human diseases, due to their effect on cellular metabolism. However, stimulation by abnormal factors, e.g., aging and toxic molecules, can alter mitochondrial energy metabolism, which consequently induces reactive oxygen species (ROS) accumulation in mitochondria (Gil et al. 2003). Once this accumulation exceeds the tolerance threshold, multiple pathological processes are initiated, including the release of additional ROS, the opening of mitochondrial membrane permeability transition pores (MPTP), oxidative stress, and mitochondrial membrane potential depolariz
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