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산화적 스트레스에 대한 석결명의 세포 보호 효과Cellular-protective effects of Nardotidis seu Sulculii Concha Extract against oxidative stress

Other Titles
Cellular-protective effects of Nardotidis seu Sulculii Concha Extract against oxidative stress
Authors
김광연이승진지선영배수진송유림윤언정박선빈송종국손태진손재동김우현양주혜박선동김상찬김영우박광일
Issue Date
May-2021
Publisher
대한한의학방제학회
Keywords
Nardotidis seu Sulculii Concha; oxidative stress; cell injury; cellular-protective effect.
Citation
대한한의학 방제학회지, v.29, no.2, pp 71 - 80
Pages
10
Indexed
KCI
Journal Title
대한한의학 방제학회지
Volume
29
Number
2
Start Page
71
End Page
80
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/5329
DOI
10.14374/HFS.2021.29.2.71
ISSN
1229-1218
2288-5641
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.
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