DOI QR코드

DOI QR Code

산화적 스트레스에 대한 석결명의 세포 보호 효과

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

  • 김광연 (한국한의학연구원) ;
  • 이승진 (동국대학교 한의과대학 방제학교실) ;
  • 지선영 (대구한의대학교 한의학과) ;
  • 배수진 (동국대학교 한의과대학 방제학교실) ;
  • 송유림 (동국대학교 한의과대학 방제학교실) ;
  • 윤언정 (동국대학교 한의과대학 방제학교실) ;
  • 박선빈 (동국대학교 한의과대학 방제학교실) ;
  • 송종국 (용인대학교) ;
  • 손태진 (경일대학교) ;
  • 손재동 (경상대학교 수의과 대학) ;
  • 김우현 (경상대학교 수의과 대학) ;
  • 양주혜 (한국한의학연구원) ;
  • 박선동 (동국대학교 한의과대학 방제학교실) ;
  • 김상찬 (대구한의대학교 한의학과) ;
  • 김영우 (동국대학교 한의과대학 방제학교실) ;
  • 박광일 (경상대학교 수의과 대학)
  • 투고 : 2021.01.13
  • 심사 : 2021.03.02
  • 발행 : 2021.05.31

초록

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.

키워드

과제정보

This research was supported by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (number: HF20C0212). This work was also supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (NRF-2017R1D1A1B03032284) (No.2019R1A2C1003200) and by grant (No. 20190055) funded by the Ministry of Oceans and Fisheries, Republic of Korea.

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