loading page

Glycopeptide from mountain-cultivated ginseng attenuates oxidant-induced cardiomyocyte and skeletal myoblast injury
  • +8
  • Dongyue Zhou,
  • Xuan Hu,
  • Tongchuan Wu,
  • Xue Li,
  • Di Yang,
  • Xingyu Tao,
  • Yunhua Fu,
  • Fei Zheng,
  • Yulin Dai,
  • Hao Yue,
  • YouJin Jeon
Dongyue Zhou
Changchun University of Chinese Medicine
Author Profile
Xuan Hu
Changchun University of Chinese Medicine
Author Profile
Tongchuan Wu
Changchun University of Chinese Medicine
Author Profile
Xue Li
Changchun University of Chinese Medicine
Author Profile
Di Yang
Changchun University of Chinese Medicine
Author Profile
Xingyu Tao
Changchun University of Chinese Medicine
Author Profile
Yunhua Fu
Changchun University of Chinese Medicine
Author Profile
Fei Zheng
Changchun University of Chinese Medicine
Author Profile
Yulin Dai
Changchun University of Chinese Medicine

Corresponding Author:[email protected]

Author Profile
Hao Yue
Changchun University of Chinese Medicine
Author Profile
YouJin Jeon
Jeju National University
Author Profile

Abstract

Background and purpose In Asian traditional medicine, ginseng has been referred to as the “King of Herbs” because to its extensive therapeutic and pharmacologic characteristics, particularly in the treatment of type 2 diabetes mellitus and illnesses connected to diabetes. Experimental approach The 80% ethanol extracts of cultivated, red, and mountain-cultivated ginseng were liquid partitioned with hexane, chloroform, ethyl acetate, and n-butanol, respectively. The residues produced were processed with enzyme-assisted extraction by different enzymes. Cardiomyocytes, skeletal myoblasts, wild-type AB line zebrafish and Tg (kdrl:EGFP) zebrafish were used to screen and verify the protective effect of extracts. Key results APMCG-1 is precipitated by alkaline protease-assisted extract from mountain-cultivated ginseng with 30% ethanol, which has a strong scavenging effect on hydroxyl radicals. In palmitic acid-induced H9c2 cells, APMCG-1 greatly enhanced cell viability while reducing reactive oxygen species generation and lactate dehydrogenase levels. Additionally, it reduced endoplasmic reticulum and mitochondrial dysfunction by increasing the Ca2+ level and membrane potential of mitochondria in H9c2(2-1) cells. In C2C12 cells that had been exposed to palmitic acid, APMCG-1 boosted glucose uptake while lowering creatine kinase levels. More significantly, 5 days after fertilization Tg (kdrl:EGFP) zebrafish and 1-month-old wild-type zebrafish with type 2 diabetic symptoms both had lower blood sugar and lipid levels attributed to APMCG-1. Further, APMCG-1 was identified as a glycopeptide containing O-linked glycopeptide bonds. Conclusions and implications As a PI3K/AKT activator, APMCG-1 protects the dysfunction of oxidant induced cardiomyocytes and skeletal myoblasts in type 2 diabetes, and is a potential therapeutic drug for diabetes.