PMID- 32050658
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 2076-3921 (Print)
IS  - 2076-3921 (Electronic)
IS  - 2076-3921 (Linking)
VI  - 9
IP  - 2
DP  - 2020 Feb 10
TI  - Lespedeza bicolor Extract Ameliorated Renal Inflammation by Regulation of NLRP3 
      Inflammasome-Associated Hyperinflammation in Type 2 Diabetic Mice.
LID - 10.3390/antiox9020148 [doi]
LID - 148
AB  - Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by 
      hyperglycemia. The chronic hyperglycemic condition causes hyperinflammation via 
      activation of nucleotide-binding oligomerization domain-like pyrin domain 
      containing receptor 3 (NLRP3) inflammasome and abnormally leads to morphological 
      and functional changes in kidney. A previous study showed a protective effect of 
      Lespedeza bicolor extract (LBE) on endothelial dysfunction induced by 
      methylglyoxal glucotoxicity. We aimed to investigate whether LBE ameliorated 
      renal damage through regulation of NLRP3 inflammasome-dependent 
      hyper-inflammation in T2DM mice. After T2DM induction by a high fat diet and low 
      dose of streptozotocin (30 mg/kg), the mice were administered with different 
      dosages of LBE (100 or 250 mg/kg/day) by gavage for 12 weeks. LBE supplementation 
      ameliorated kidney dysfunction demonstrated by urine albumin-creatinine at a low 
      dose and plasma creatinine, blood urea nitrogen (BUN), and glomerular hypertrophy 
      at a high dose. Furthermore, a high dose of LBE supplementation significantly 
      attenuated renal hyper-inflammation associated with NLRP3 inflammasome and 
      oxidative stress related to nuclear factor erythroid 2-related factor 2 (Nrf-2) 
      in T2DM mice. Meanwhile, a low dose of LBE supplementation up-regulated energy 
      metabolism demonstrated by phosphorylation of adenosine monophosphate kinase 
      (AMPK) and Sirtuin (SIRT)-1 in T2DM mice. In conclusion, the current study 
      suggested that LBE, in particular, at a high dose could be used as a beneficial 
      therapeutic for hyperglycemia-induced renal damage in T2DM.
FAU - Park, Ji Eun
AU  - Park JE
AD  - Department of Food and Nutrition, Kyung Hee Univerity, 26 Kyung Hee-Daero, 
      Dongdamun-Gu, Seoul 02447, Korea.
FAU - Lee, Heaji
AU  - Lee H
AD  - Department of Food and Nutrition, Kyung Hee Univerity, 26 Kyung Hee-Daero, 
      Dongdamun-Gu, Seoul 02447, Korea.
FAU - Kim, Sun Yeou
AU  - Kim SY
AD  - Gachon Institute of Pharmaceutical Science, Gachon University, #191, Hambakmoero, 
      Yeonsu-gu, Incheon 21936, Korea.
FAU - Lim, Yunsook
AU  - Lim Y
AD  - Department of Food and Nutrition, Kyung Hee Univerity, 26 Kyung Hee-Daero, 
      Dongdamun-Gu, Seoul 02447, Korea.
LA  - eng
GR  - 2018R1D1A1B07046778/Ministry of Education, Science and Technology/
PT  - Journal Article
DEP - 20200210
PL  - Switzerland
TA  - Antioxidants (Basel)
JT  - Antioxidants (Basel, Switzerland)
JID - 101668981
PMC - PMC7071116
OTO - NOTNLM
OT  - Lespedeza bicolor
OT  - NLRP3 inflammasome
OT  - energy metabolism
OT  - oxidative stress
OT  - renal inflammation
OT  - type 2 diabetes
COIS- Tumor necrosis factor alpha
EDAT- 2020/02/14 06:00
MHDA- 2020/02/14 06:01
PMCR- 2020/02/10
CRDT- 2020/02/14 06:00
PHST- 2019/12/18 00:00 [received]
PHST- 2020/01/29 00:00 [revised]
PHST- 2020/02/05 00:00 [accepted]
PHST- 2020/02/14 06:00 [entrez]
PHST- 2020/02/14 06:00 [pubmed]
PHST- 2020/02/14 06:01 [medline]
PHST- 2020/02/10 00:00 [pmc-release]
AID - antiox9020148 [pii]
AID - antioxidants-09-00148 [pii]
AID - 10.3390/antiox9020148 [doi]
PST - epublish
SO  - Antioxidants (Basel). 2020 Feb 10;9(2):148. doi: 10.3390/antiox9020148.