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2.
Chin J Physiol ; 65(6): 282-289, 2022.
Article in English | MEDLINE | ID: mdl-36588354

ABSTRACT

Spinal cord injury (SCI) is a common central nervous system disease. It is reported that long non-coding RNA LINC00158 is involved in the process of SCI. The purpose of this study was to explore the biological role of LINC00158 in the SCI. First, we established a rat SCI model by surgical method and evaluated the motor function of rats by the Basso-Beattie-Bresnahan locomotor rating scale. The results showed that the expression of LINC00158 decreased and apoptotic cells increased in the SCI model rats. Meanwhile, we found the upregulated LC3-II/LC3-I, Beclin-1, and p62 in the SCI rats. Then, primary rat spinal cord neurons were exposed to oxygen/glucose deprivation (OGD) as an in vitro cell model of SCI. After OGD treatment, the expression of LINC00158 decreased significantly and the apoptosis of spinal cord neurons increased. OGD treatment resulted in upregulation of LC3-II/LC3-I and Beclin-1 and downregulation of p62 in primary spinal cord neurons, which could be eliminated by overexpression of LINC00158. 3-Methyladenine and chloroquine (autophagy inhibitor) reversed the inhibitory effect of LINC00158 overexpression on apoptosis of primary spinal cord neurons. In conclusion, this study demonstrated that LINC00158 overexpression repressed neuronal apoptosis by promoting autophagy, suggesting that LINC00158 may be a potential therapeutic target in the SCI.


Subject(s)
RNA, Long Noncoding , Spinal Cord Injuries , Rats , Animals , RNA, Long Noncoding/genetics , RNA, Long Noncoding/metabolism , RNA, Long Noncoding/pharmacology , Rats, Sprague-Dawley , Beclin-1/genetics , Beclin-1/metabolism , Beclin-1/pharmacology , Spinal Cord Injuries/drug therapy , Spinal Cord Injuries/metabolism , Spinal Cord/metabolism , Apoptosis , Autophagy
3.
J Sci Food Agric ; 98(2): 590-597, 2018 Jan.
Article in English | MEDLINE | ID: mdl-28664987

ABSTRACT

BACKGROUND: The aim of this study was to investigate in vitro antioxidant activities and cytoprotective effect of Maillard reaction products (MRPs) from phloridzin (Pz)-amino acid model systems. Their structures were also characterised by Fourier transform-infrared spectroscopy (FTIR). RESULTS: MRPs were prepared from the Pz-methionine (Met), Pz-lysine (Lys), Pz-isoleucine (Ile), Pz-histidine (His) or Pz-glutamic acid (Glu) model system. The Pz-Lys MRPs, rich in antioxidant potency, were subjected to ultrafiltration to yield four MRPs fractions with different molecular weights (Mw). The fraction with Mw 30-50 kDa had significantly (P < 0.05) higher antioxidant activity than other fractions. Moreover, it significantly (P < 0.05) attenuated the 2,2'-azobis(2-methylpropionamidine) dihydrochloride (AAPH)-elicited decrease in cell viability in HepG2 cells in a concentration-dependent manner. FTIR analysis indicated that the fraction with Mw 30-50 kDa had the strong stretching vibration for the OH, NH, CH, CO and CC groups, suggesting the formation of intermediate MRPs during Maillard reaction. CONCLUSION: The results obtained in this study may provide some basis for the purported health-promoting effects of MRPs and their potential application as antioxidant agents in food industry. Also, it is important for our understanding of the variation of bioactive substances in food during thermal processing. © 2017 Society of Chemical Industry.


Subject(s)
Amino Acids/chemistry , Antioxidants/chemistry , Glycation End Products, Advanced/chemistry , Phlorhizin/chemistry , Protective Agents/chemistry , Antioxidants/pharmacology , Cell Survival/drug effects , Glycation End Products, Advanced/pharmacology , Hep G2 Cells , Humans , Maillard Reaction , Oxidation-Reduction , Protective Agents/pharmacology
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