Abstract
Heat stress can be caused by various environmental factors. When exposed to heat stress, oxidative stress and inflammatory reaction occur due to an increase of reactive oxygen species (ROS) in the body. In particular, inflammatory responses induced by heat stress are common in muscle cells, which are the most exposed to heat stress and directly affected. Gintonin-Enriched Fraction (GEF) is a non-saponin component of ginseng, a glycolipoprotein. It is known that it has excellent neuroprotective effects, therefore, we aimed to confirm the protective effect against heat stress by using GEF. C2C12 cells were exposed to high temperature stress for 1, 12 and 15 h, and the expression of signals was analyzed over time. Changes in the expression of the factors that were observed under heat stress were confirmed at the protein level. Exposure to heat stress increases phosphorylation of p38 and extracellular signal-regulated kinase (ERK) and increases expression of inflammatory factors such as NLRP3 inflammasome through lysophosphatidic acid (LPA) receptor. Activated inflammatory signals also increase the secretion of inflammatory cytokines such as interleukin 6 (IL-6) and interleukin 18 (IL-18). Also, expression of glutathione reductase (GR) and catalase related to oxidative stress is increased. However, it was confirmed that the changes due to the heat stress were suppressed by the GEF treatment. Therefore, we suggest that GEF helps to protect heat stress in muscle cell and prevent tissue damage by oxidative stress and inflammation.
Highlights
High temperature environments such as those due to global warming or hot summer seasons causes heat stress, which generates reactive oxygen species (ROS) and causes oxidative stress [1].Oxidative stress is caused by an imbalance between the production of reactive oxygen species in the body and the ability of the biological system to remove them [2]
To determine whether heat stress affects the mitogen-activated protein kinase (MAPK) signaling pathway in C2C12 cells, phosphorylation of p38 and extracellular signal-regulated kinase (ERK) was confirmed in cells exposed to heat stress for 1 h
In order to suppress oxidative stress and inflammatory reaction due to heat stress, the effect of C2C12 cells was confirmed by using Gintonin-Enriched Fraction (GEF)
Summary
High temperature environments such as those due to global warming or hot summer seasons causes heat stress, which generates reactive oxygen species (ROS) and causes oxidative stress [1]. Oxidative stress is caused by an imbalance between the production of reactive oxygen species in the body and the ability of the biological system to remove them [2]. The redox imbalance of cells can cause toxic effects through the production of peroxides and free radicals that damage all components of the cell, including proteins, lipids, and DNA [3]. Oxidative stress caused by oxidative metabolism causes DNA strand breakage, and base damage [4]. Since oxidative stress induces cytotoxicity and cell destruction, it is important that it be properly regulated. Innate immune function can be prevented by pattern recognition receptors (PRRs) from pathogen-associated molecular pattern (PAMPs) induced by pathogen invasion
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