PMID- 37385299
OWN - NLM
STAT- MEDLINE
DCOM- 20230915
LR  - 20231004
IS  - 1872-9711 (Electronic)
IS  - 0161-813X (Linking)
VI  - 98
DP  - 2023 Sep
TI  - Isochlorogenic acid B alleviates lead-induced anxiety, depression and 
      neuroinflammation in mice by the BDNF pathway.
PG  - 1-8
LID - S0161-813X(23)00087-6 [pii]
LID - 10.1016/j.neuro.2023.06.007 [doi]
AB  - Lead (Pb) can cause neurobehavioral abnormalities. Isochlorogenic acid B (ICAB), 
      a dietary flavonoid found in tea, sweet potato, artichoke, propolis and several 
      plants, exhibited potential neuroprotective properties. In this study, we aimed 
      to investigate the mechanisms of Pb-induced anxiety, depression and 
      neuroinflammation, and the neuroprotective effect of ICAB in mouse brains. We 
      found that ICAB supplementation significantly improved behavioral abnormalities, 
      neuroinflammation and oxidative stress induced by Pb. ICAB attenuated Pb-induced 
      anxiety and depression behavior in mice, as indicated by decreasing the duration 
      of immobility in tail suspension test and increasing the crossing number, rearing 
      number and time in center in open field test. Accordingly, ICAB inhibited 
      oxidative stress by decreasing malondialdehyde (MDA) level and increasing the 
      antioxidant enzyme activity. ICAB also inhibited Pb-induced inflammation in 
      brain, as indicated by decreasing the tumor necrosis factor-alpha (TNF-alpha) and 
      interleukin-6 (IL-6) levels. ICAB increased the expression levels of brain 
      derived neurotrophic factor (BDNF) and the phosphorylation of cAMP-responsive 
      element binding protein (CREB), phosphoinositide 3-kinases-protein kinase B 
      (PI3K/AKT). Furthermore, ICAB decreased the levels of Toll-like receptor 4 
      (TLR4), myeloid differentiation factor 88 (MyD88), glycogen synthase kinase-3 
      beta (GSK-3beta) and p38. Collectively, this study demonstrated that ICAB improved 
      Pb-induced anxiety, depression, neuroinflammation and oxidative stress by 
      regulating the BDNF signaling pathway.
CI  - Copyright (c) 2023 Elsevier B.V. All rights reserved.
FAU - Shi, Jia-Xue
AU  - Shi JX
AD  - School of Life Science, Jiangsu Normal University, No.101, Shanghai Road, 
      Tongshan New Area, 21-1116 Xuzhou City, Jiangsu Province, PR China.
FAU - Cheng, Chao
AU  - Cheng C
AD  - School of Life Science, Jiangsu Normal University, No.101, Shanghai Road, 
      Tongshan New Area, 21-1116 Xuzhou City, Jiangsu Province, PR China.
FAU - Ruan, Hai-Nan
AU  - Ruan HN
AD  - School of Life Science, Jiangsu Normal University, No.101, Shanghai Road, 
      Tongshan New Area, 21-1116 Xuzhou City, Jiangsu Province, PR China.
FAU - Li, Jun
AU  - Li J
AD  - School of Life Science, Jiangsu Normal University, No.101, Shanghai Road, 
      Tongshan New Area, 21-1116 Xuzhou City, Jiangsu Province, PR China.
FAU - Liu, Chan-Min
AU  - Liu CM
AD  - School of Life Science, Jiangsu Normal University, No.101, Shanghai Road, 
      Tongshan New Area, 21-1116 Xuzhou City, Jiangsu Province, PR China. Electronic 
      address: lcm9009@126.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20230628
PL  - Netherlands
TA  - Neurotoxicology
JT  - Neurotoxicology
JID - 7905589
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta)
RN  - 2P299V784P (Lead)
RN  - E57A0DKE0B (3,4-di-O-caffeoylquinic acid)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - 0 (Antioxidants)
SB  - IM
MH  - Mice
MH  - Animals
MH  - *Depression/chemically induced/drug therapy/prevention & control
MH  - *Brain-Derived Neurotrophic Factor/metabolism
MH  - Glycogen Synthase Kinase 3 beta
MH  - Lead/toxicity
MH  - Neuroinflammatory Diseases
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Anxiety/chemically induced/drug therapy/prevention & control
MH  - Antioxidants
OTO - NOTNLM
OT  - BDNF
OT  - Depression
OT  - Inflammation
OT  - Isochlorogenic acid B
OT  - Lead
OT  - Oxidative stress
COIS- Declaration of Competing Interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2023/06/30 01:06
MHDA- 2023/09/15 06:42
CRDT- 2023/06/29 19:12
PHST- 2023/05/03 00:00 [received]
PHST- 2023/06/23 00:00 [revised]
PHST- 2023/06/25 00:00 [accepted]
PHST- 2023/09/15 06:42 [medline]
PHST- 2023/06/30 01:06 [pubmed]
PHST- 2023/06/29 19:12 [entrez]
AID - S0161-813X(23)00087-6 [pii]
AID - 10.1016/j.neuro.2023.06.007 [doi]
PST - ppublish
SO  - Neurotoxicology. 2023 Sep;98:1-8. doi: 10.1016/j.neuro.2023.06.007. Epub 2023 Jun 
      28.