PMID- 33153341
OWN - NLM
STAT- MEDLINE
DCOM- 20211231
LR  - 20211231
IS  - 1460-2202 (Electronic)
IS  - 0271-3683 (Linking)
VI  - 46
IP  - 6
DP  - 2021 Jun
TI  - Alginate Oligosaccharide Prevents against D-galactose-mediated Cataract in 
      C57BL/6J Mice via Regulating Oxidative Stress and Antioxidant System.
PG  - 802-810
LID - 10.1080/02713683.2020.1842456 [doi]
AB  - PURPOSE: Alginate oligosaccharides (AOS), obtained from depolymerizing alginate, 
      has multiple pharmacological benefits. Cataract is a common disease caused by 
      turbidity of the lens protein due to lens metabolism disorders. This study aimed 
      to test the effects and the underlying mechanisms of AOS on D-galactose 
      (D-gal)-mediated cataract. MATERIALS AND METHODS: A total of 45 8-week-old 
      C57BL/6 J male mice were randomly divided into 5 groups. After eight weeks' 
      intervention, the score of cataract was calculated depending on the turbidity of 
      the lens. Hematoxylin and eosin (HE) and transmission electron microscope (TEM) 
      images were observed. Superoxide dismutase (SOD) activity and malondialdehyde 
      (MDA) level were measured by corresponding detection kits, respectively. SOD1, 
      SOD2, catalase (CAT) and p53 protein expressions were examined by Western blot. 
      Nuclear factor erythroid-2 related factor (Nrf2) and heme oxygenase-1 (HO-1) mRNA 
      expressions were examined by Quantitative Real Time-PCR (RT-qPCR). RESULTS: The 
      score of the turbidity of the lens showed that AOS significantly delayed the 
      cataractogenesis. HE staining and TEM imaging showed that AOS decreased the 
      damage and senescence of lenses in D-gal-induced C57BL/6 J mice. We further 
      detected aging marker p53 expression in crystalline lenses, and our result showed 
      that AOS significantly inhibited p53 protein expression in D-gal-induced mice. In 
      addition, SOD activity and MDA level detection results showed that AOS 
      significantly increased the activity of SOD, and decreased the level of MDA in 
      crystalline lenses homogenates of D-gal-induced aging mice. Western blot results 
      showed that AOS attenuated the damage of D-gal in the protein expressions of 
      antioxidative enzymes SOD1, SOD2 and CAT. RT-qPCR results showed that AOS 
      suppressed the down-regulation of Nrf2 and HO-1 mRNA expressions induced by 
      D-gal. CONCLUSIONS: AOS prevents against D-gal-mediated cataract in C57BL/6 J 
      mice via inhibiting oxidative stress and up-regulating antioxidant system. 
      Consequently, our results suggest that AOS may be an effective therapeutic 
      strategy against cataract.
FAU - Feng, Wenjing
AU  - Feng W
AD  - Department of Geriatric Medicine, The Affiliated Hospital of Qingdao University, 
      Qingdao, China.
AD  - Department of Epidemiology and Health Statistics, The School of Public Health of 
      Qingdao University, Qingdao, Shandong, China.
FAU - Yang, Xuejiao
AU  - Yang X
AD  - Department of Ophthalmology, The Affiliated Hospital of Qingdao University, 
      Qingdao, China.
FAU - Feng, Meiping
AU  - Feng M
AD  - Department of Geriatric Medicine, The Affiliated Hospital of Qingdao University, 
      Qingdao, China.
FAU - Pan, Hui
AU  - Pan H
AD  - Department of Geriatric Medicine, The Affiliated Hospital of Qingdao University, 
      Qingdao, China.
FAU - Liu, Jianya
AU  - Liu J
AD  - Department of Geriatric Medicine, The Affiliated Hospital of Qingdao University, 
      Qingdao, China.
FAU - Hu, Yi
AU  - Hu Y
AD  - Department of Geriatric Medicine, The Affiliated Hospital of Qingdao University, 
      Qingdao, China.
FAU - Wang, Shan
AU  - Wang S
AD  - Department of Geriatric Medicine, The Affiliated Hospital of Qingdao University, 
      Qingdao, China.
FAU - Zhang, Dongfeng
AU  - Zhang D
AD  - Department of Epidemiology and Health Statistics, The School of Public Health of 
      Qingdao University, Qingdao, Shandong, China.
FAU - Ma, Fenghua
AU  - Ma F
AD  - Department of Geriatric Medicine, The Affiliated Hospital of Qingdao University, 
      Qingdao, China.
FAU - Mao, Yongjun
AU  - Mao Y
AD  - Department of Geriatric Medicine, The Affiliated Hospital of Qingdao University, 
      Qingdao, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20201106
PL  - England
TA  - Curr Eye Res
JT  - Current eye research
JID - 8104312
RN  - 0 (Alginates)
RN  - 0 (Antioxidants)
RN  - 0 (Membrane Proteins)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (Nfe2l2 protein, mouse)
RN  - 0 (Oligosaccharides)
RN  - 0 (RNA, Messenger)
RN  - 0 (Trp53 protein, mouse)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 1.11.1.6 (Catalase)
RN  - EC 1.14.14.18 (Heme Oxygenase-1)
RN  - EC 1.14.14.18 (Hmox1 protein, mouse)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - X2RN3Q8DNE (Galactose)
SB  - IM
MH  - Alginates/*pharmacology
MH  - Animals
MH  - Antioxidants/*metabolism
MH  - Blotting, Western
MH  - Catalase/metabolism
MH  - Cataract/chemically induced/metabolism/*prevention & control
MH  - Galactose/*toxicity
MH  - Heme Oxygenase-1/genetics
MH  - Lens, Crystalline/*drug effects/metabolism/ultrastructure
MH  - Male
MH  - Malondialdehyde/metabolism
MH  - Membrane Proteins/genetics
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Microscopy, Electron, Transmission
MH  - NF-E2-Related Factor 2/genetics
MH  - Oligosaccharides/*pharmacology
MH  - Oxidative Stress/*physiology
MH  - RNA, Messenger/genetics
MH  - Real-Time Polymerase Chain Reaction
MH  - Superoxide Dismutase/metabolism
MH  - Tumor Suppressor Protein p53/metabolism
OTO - NOTNLM
OT  - Cataract
OT  - D-galactose
OT  - aging
OT  - alginate oligosaccharide
OT  - oxidative stress
EDAT- 2020/11/07 06:00
MHDA- 2022/01/01 06:00
CRDT- 2020/11/06 05:35
PHST- 2020/11/07 06:00 [pubmed]
PHST- 2022/01/01 06:00 [medline]
PHST- 2020/11/06 05:35 [entrez]
AID - 10.1080/02713683.2020.1842456 [doi]
PST - ppublish
SO  - Curr Eye Res. 2021 Jun;46(6):802-810. doi: 10.1080/02713683.2020.1842456. Epub 
      2020 Nov 6.