PMID- 32245940
OWN - NLM
STAT- MEDLINE
DCOM- 20200409
LR  - 20200415
IS  - 1643-3750 (Electronic)
IS  - 1234-1010 (Print)
IS  - 1234-1010 (Linking)
VI  - 26
DP  - 2020 Apr 4
TI  - Ganoderma Lucidum Polysaccharides Ameliorates Hepatic Steatosis and Oxidative 
      Stress in db/db Mice via Targeting Nuclear Factor E2 (Erythroid-Derived 
      2)-Related Factor-2/Heme Oxygenase-1 (HO-1) Pathway.
PG  - e921905
LID - 10.12659/MSM.921905 [doi]
AB  - BACKGROUND Type 2 diabetes mellitus (T2DM) and its comorbidities, including 
      obesity, hypertension, and hyperlipidemia, are commonly associated with 
      non-alcoholic fatty liver disease (NAFLD). Ganoderma lucidum polysaccharide 
      (GDLP) is one of the central bioactive components in Ganoderma lucidum with 
      anti-inflammatory, antioxidant, and hepatoprotective properties. However, the 
      effect and mechanisms of GDLP in hepatic steatosis remain largely unknown. In the 
      present study, we aimed to investigate the function of GDLP in hepatic steatosis 
      and the underlying mechanism. MATERIAL AND METHODS In this study, male db/db mice 
      were received with a high-fat diet (HFD) to investigate the effect of GDLP in 
      T2DM-induced hepatic steatosis. The biological characteristics of the hepatic 
      steatosis were evaluated through the detection of clinical indicators, including 
      biochemical parameters, histopathology, and related cytokine levels. 
      Additionally, the protein expression levels of Nrf2 (nuclear factor E2 
      (erythroid-derived 2)-related factor-2) signaling pathway were investigated by 
      using western blotting and immunohistochemical staining. RESULTS The levels of 
      food/water intake, body weight, fasting blood glucose, plasma lipids, urinary 
      biomarkers, hepatic lipid accumulation, and tumor necrosis factor (TNF)-alpha 
      were observably decreased in GDLP-treated db/db mice. Additionally, 
      administration of GDLP increased the expression of various antioxidases, 
      including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase 
      (GSH-Px), whereas it reduced the level of malonaldehyde (MDA). Furthermore, GDLP 
      was significantly promoted protein expression level of Nrf2 and its downstream 
      target gene HO-1 (heme oxygenase-1) while decreased TNF-alpha expression. 
      CONCLUSIONS These results indicate that GDLP against T2DM-induced hepatic 
      steatosis, oxidative stress, and inflammation by improving the Nrf2/HO-1 
      signaling pathway in db/db mice, suggesting the GDLP may serve as an effective 
      strategy for in fatty liver treatment.
FAU - Li, Hong Ning
AU  - Li HN
AD  - Zhejiang University School of Medicine, Hangzhou, Zhejiang, China (mainland).
FAU - Zhao, Ling Li
AU  - Zhao LL
AD  - Hangzhou AIMA Maternity Hospital, Hangzhou, Zhejiang, China (mainland).
FAU - Zhou, Di Yi
AU  - Zhou DY
AD  - Zhejiang Integrated Traditional and Western Medicine Hospital, Hangzhou, 
      Zhejiang, China (mainland).
FAU - Chen, Dan Qing
AU  - Chen DQ
AD  - Women Hospital School of Medicine Zhejiang University, Hangzhou, Zhejiang, China 
      (mainland).
LA  - eng
PT  - Journal Article
DEP - 20200404
PL  - United States
TA  - Med Sci Monit
JT  - Medical science monitor : international medical journal of experimental and 
      clinical research
JID - 9609063
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (Polysaccharides)
RN  - EC 1.14.14.18 (Heme Oxygenase-1)
SB  - IM
MH  - Animals
MH  - Diabetes Mellitus, Type 2/complications/metabolism
MH  - Fatty Liver/*drug therapy
MH  - Heme Oxygenase-1/*metabolism
MH  - Male
MH  - Mice
MH  - NF-E2-Related Factor 2/*metabolism
MH  - Oxidative Stress/*drug effects
MH  - Polysaccharides
MH  - Reishi/*chemistry
PMC - PMC7154563
COIS- Conflict of interests None.
EDAT- 2020/04/05 06:00
MHDA- 2020/04/10 06:00
PMCR- 2020/04/04
CRDT- 2020/04/05 06:00
PHST- 2020/04/05 06:00 [entrez]
PHST- 2020/04/05 06:00 [pubmed]
PHST- 2020/04/10 06:00 [medline]
PHST- 2020/04/04 00:00 [pmc-release]
AID - 921905 [pii]
AID - 10.12659/MSM.921905 [doi]
PST - epublish
SO  - Med Sci Monit. 2020 Apr 4;26:e921905. doi: 10.12659/MSM.921905.