PMID- 32106493 OWN - NLM STAT- MEDLINE DCOM- 20201201 LR - 20201201 IS - 1420-3049 (Electronic) IS - 1420-3049 (Linking) VI - 25 IP - 5 DP - 2020 Feb 25 TI - Gintonin-Enriched Fraction Suppresses Heat Stress-Induced Inflammation Through LPA Receptor. LID - 10.3390/molecules25051019 [doi] LID - 1019 AB - 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. FAU - Chei, Sungwoo AU - Chei S AD - Department of Biomedical Sciences, CHA University, Seongnam-si 13488, Gyeonggi-do, Korea. FAU - Song, Ji-Hyeon AU - Song JH AD - Department of Biomedical Sciences, CHA University, Seongnam-si 13488, Gyeonggi-do, Korea. FAU - Oh, Hyun-Ji AU - Oh HJ AD - Department of Biomedical Sciences, CHA University, Seongnam-si 13488, Gyeonggi-do, Korea. FAU - Lee, Kippeum AU - Lee K AD - Department of Biomedical Sciences, CHA University, Seongnam-si 13488, Gyeonggi-do, Korea. FAU - Jin, Heegu AU - Jin H AD - Department of Biomedical Sciences, CHA University, Seongnam-si 13488, Gyeonggi-do, Korea. FAU - Choi, Sun-Hye AU - Choi SH AD - Ginsentology Research Laboratory and Department of Physiology, College of Veterinary Medicine, Konkuk University, Seoul 05029, Korea. FAU - Nah, Seung-Yeol AU - Nah SY AD - Ginsentology Research Laboratory and Department of Physiology, College of Veterinary Medicine, Konkuk University, Seoul 05029, Korea. FAU - Lee, Boo-Yong AU - Lee BY AD - Department of Biomedical Sciences, CHA University, Seongnam-si 13488, Gyeonggi-do, Korea. LA - eng PT - Journal Article DEP - 20200225 PL - Switzerland TA - Molecules JT - Molecules (Basel, Switzerland) JID - 100964009 RN - 0 (Neuroprotective Agents) RN - 0 (Plant Extracts) RN - 0 (Reactive Oxygen Species) RN - 0 (Receptors, Lysophosphatidic Acid) RN - 0 (gintonin) RN - SY7Q814VUP (Calcium) SB - IM MH - Animals MH - Calcium/metabolism MH - Cell Line MH - Heat-Shock Response/drug effects/physiology MH - Humans MH - Inflammation/*drug therapy MH - Mice MH - Neuroprotective Agents/chemistry/pharmacology MH - Oxidative Stress/drug effects MH - Panax/*chemistry MH - Plant Extracts/chemistry/*pharmacology MH - Reactive Oxygen Species/metabolism MH - Receptors, Lysophosphatidic Acid/*genetics PMC - PMC7179209 OTO - NOTNLM OT - C2C12 cell OT - ginseng OT - gintonin OT - gintonin-enriched fraction (GEF) OT - heat stress OT - inflammation COIS- The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results. EDAT- 2020/02/29 06:00 MHDA- 2020/12/02 06:00 PMCR- 2020/02/25 CRDT- 2020/02/29 06:00 PHST- 2020/01/10 00:00 [received] PHST- 2020/02/20 00:00 [revised] PHST- 2020/02/21 00:00 [accepted] PHST- 2020/02/29 06:00 [entrez] PHST- 2020/02/29 06:00 [pubmed] PHST- 2020/12/02 06:00 [medline] PHST- 2020/02/25 00:00 [pmc-release] AID - molecules25051019 [pii] AID - molecules-25-01019 [pii] AID - 10.3390/molecules25051019 [doi] PST - epublish SO - Molecules. 2020 Feb 25;25(5):1019. doi: 10.3390/molecules25051019.