PMID- 35142690
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220309
IS  - 1673-5374 (Print)
IS  - 1876-7958 (Electronic)
IS  - 1673-5374 (Linking)
VI  - 17
IP  - 9
DP  - 2022 Sep
TI  - Urolithin A alleviates blood-brain barrier disruption and attenuates neuronal 
      apoptosis following traumatic brain injury in mice.
PG  - 2007-2013
LID - 10.4103/1673-5374.335163 [doi]
AB  - Urolithin A (UA) is a natural metabolite produced from polyphenolics in foods 
      such as pomegranates, berries, and nuts. UA is neuroprotective against 
      Parkinson's disease, Alzheimer's disease, and cerebral hemorrhage. However, its 
      effect against traumatic brain injury remains unknown. In this study, we 
      established adult C57BL/6J mouse models of traumatic brain injury by controlled 
      cortical impact and then intraperitoneally administered UA. We found that UA 
      greatly reduced brain edema; increased the expression of tight junction proteins 
      in injured cortex; increased the immunopositivity of two neuronal autophagy 
      markers, microtubule-associated protein 1A/B light chain 3A/B (LC3) and p62; 
      downregulated protein kinase B (Akt) and mammalian target of rapamycin (mTOR), 
      two regulators of the phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR signaling 
      pathway; decreased the phosphorylation levels of inhibitor of NFkappaB (IkappaB) kinase 
      alpha (IKKalpha) and nuclear factor kappa B (NFkappaB), two regulators of the 
      neuroinflammation-related Akt/IKK/NFkappaB signaling pathway; reduced blood-brain 
      barrier permeability and neuronal apoptosis in injured cortex; and improved mouse 
      neurological function. These findings suggest that UA may be a candidate drug for 
      the treatment of traumatic brain injury, and its neuroprotective effects may be 
      mediated by inhibition of the PI3K/Akt/mTOR and Akt/IKK/NFkappaB signaling pathways, 
      thus reducing neuroinflammation and enhancing autophagy.
FAU - Gong, Qiu-Yuan
AU  - Gong QY
AD  - Department of Neurosurgery, Shanghai Jiao Tong University Affiliated Sixth 
      People's Hospital, Shanghai, China.
FAU - Cai, Lin
AU  - Cai L
AD  - Department of Neurosurgery, Shanghai Jiao Tong University Affiliated Sixth 
      People's Hospital, Shanghai, China.
FAU - Jing, Yao
AU  - Jing Y
AD  - Department of Neurosurgery, Shanghai Jiao Tong University Affiliated Sixth 
      People's Hospital, Shanghai, China.
FAU - Wang, Wei
AU  - Wang W
AD  - Department of Neurosurgery, Shanghai Jiao Tong University Affiliated Sixth 
      People's Hospital, Shanghai, China.
FAU - Yang, Dian-Xu
AU  - Yang DX
AD  - Department of Neurosurgery, Shanghai Jiao Tong University Affiliated Sixth 
      People's Hospital, Shanghai, China.
FAU - Chen, Shi-Wen
AU  - Chen SW
AD  - Department of Neurosurgery, Shanghai Jiao Tong University Affiliated Sixth 
      People's Hospital, Shanghai, China.
FAU - Tian, Heng-Li
AU  - Tian HL
AD  - Department of Neurosurgery, Shanghai Jiao Tong University Affiliated Sixth 
      People's Hospital, Shanghai, China.
LA  - eng
PT  - Journal Article
PL  - India
TA  - Neural Regen Res
JT  - Neural regeneration research
JID - 101316351
PMC - PMC8848621
OTO - NOTNLM
OT  - autophagy
OT  - blood-brain barrier
OT  - cerebral edema
OT  - controlled cortical impact model
OT  - neuronal apoptosis
OT  - neuropharmacology
OT  - neuroprotection
OT  - tight junction protein
OT  - traumatic brain injury
OT  - urolithin A
COIS- None
EDAT- 2022/02/11 06:00
MHDA- 2022/02/11 06:01
PMCR- 2022/02/08
CRDT- 2022/02/10 12:14
PHST- 2022/02/10 12:14 [entrez]
PHST- 2022/02/11 06:00 [pubmed]
PHST- 2022/02/11 06:01 [medline]
PHST- 2022/02/08 00:00 [pmc-release]
AID - NeuralRegenRes_2022_17_9_2007_335163 [pii]
AID - NRR-17-2007 [pii]
AID - 10.4103/1673-5374.335163 [doi]
PST - ppublish
SO  - Neural Regen Res. 2022 Sep;17(9):2007-2013. doi: 10.4103/1673-5374.335163.