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http://dx.doi.org/10.14374/HFS.2021.29.2.71

Cellular-protective effects of Nardotidis seu Sulculii Concha Extract against oxidative stress  

Kim, Kwang Yeon (Korea Institute of Oriental Medicine)
Lee, Seung Jin (School of Korean Medicine, Dongguk University)
Jee, Seon Young (College of Korean Medicine, Daegu Haany University)
Bae, Su Jin (School of Korean Medicine, Dongguk University)
Song, Yu Rim (School of Korean Medicine, Dongguk University)
Yun, Un-Jung (School of Korean Medicine, Dongguk University)
Bak, Seonbeen (School of Korean Medicine, Dongguk University)
Song, Jong Kuk (Yong In University)
Son, Tae Jin (Kyung Il University)
Son, Jae-Dong (College of Veterinary Medicine, Gyeongsang National University)
Kim, Woo Hyun (College of Veterinary Medicine, Gyeongsang National University)
Yang, Ju Hye (Korea Institute of Oriental Medicine)
Park, Sun Dong (School of Korean Medicine, Dongguk University)
Kim, Sang Chan (College of Korean Medicine, Daegu Haany University)
Kim, Young Woo (School of Korean Medicine, Dongguk University)
Park, Kwang-Il (College of Veterinary Medicine, Gyeongsang National University)
Publication Information
Herbal Formula Science / v.29, no.2, 2021 , pp. 71-80 More about this Journal
Abstract
Objectives : This study investigated cellular-protective effects of Nardotidis seu Sulculii Concha water extract (NSCE) against oxidative stress induced by arachidonic acid (AA)+iron or tert-butylhydroperoxide (tBHP). Methods : In vitro, MTT assay was assessed for cell viability, and immunoblotting analysis was performed to detect expression of AMP-activated kinase (AMPK) signaling pathway and autophagy related proteins. In vivo, mice were orally administrated with the aqueous extract of NSCE of 500 mg/kg for 3 days, and then injected with CCl4 0.5 mg/kg body weight to induce acute damage. The level of liver damage was measured by serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) analysis. Results : Treatment with NSCE inhibited cell death induced by AA+iron and tBHP. NSCE induced the phosphorylation of AMPK, and this compound also induced the phosphorylation of LKB1, an upstream kinase of AMPK, and Acetyl-CoA carboxylase (ACC), a primary downstream target of AMPK. NSCE increased the protein levels of autophagic markers (LC3II and beclin-1) and decreased the phosphorylation of mammalian target of rapamycin (mTOR) and simultaneously increased the phosphorylation of unc-51-like kinase-1 (ULK-1) in time-dependent manner. Conclusions : NSCE has the ability 1) to protect cells against oxidative stress induced by AA+iron or tBHP. NSCE 2) to activate AMP-activated protein kinase (AMPK), and 3) to regulate autophagy, an important regulator in cell survival.
Keywords
Nardotidis seu Sulculii Concha; oxidative stress; cell injury; cellular-protective effect;
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Times Cited By KSCI : 2  (Citation Analysis)
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