PMID- 31515728
OWN - NLM
STAT- MEDLINE
DCOM- 20210201
LR  - 20210201
IS  - 1559-1174 (Electronic)
IS  - 1535-1084 (Linking)
VI  - 21
IP  - 4
DP  - 2019 Dec
TI  - Acetyl-11-keto-beta-boswellic acid (AKBA) Attenuates Oxidative Stress, Inflammation, 
      Complement Activation and Cell Death in Brain Endothelial Cells Following 
      OGD/Reperfusion.
PG  - 505-516
LID - 10.1007/s12017-019-08569-z [doi]
AB  - Brain endothelial cells play an important role in maintaining blood flow 
      homeostasis in the brain. Cerebral ischemia is a major cause of endothelial 
      dysfunction which can disrupt the blood-brain barrier (BBB). Oxygen-glucose 
      deprivation (OGD)/reperfusion promote cell death and BBB breakdown in brain 
      endothelial cells. Acetyl-11-keto-beta-boswellic acid (AKBA), a biologically active 
      phytoconstituent of the medicinal plant Boswellia serrata, has been shown to be 
      protective against various inflammatory diseases as well as ischemic brain 
      injury. The molecular mechanisms underlying these beneficial characteristics of 
      AKBA are poorly understood. We subjected bEND.3 cells to OGD/reperfusion to 
      investigate the protective role of AKBA in this model. We found that AKBA 
      treatment attenuated endothelial cell death and oxidative stress assessed by 
      means of TUNEL assay, cleaved-caspase-3, and dihydroethidium (DHE) staining. 
      Furthermore, OGD downregulated tight junction proteins ZO-1 and Occludin levels, 
      and increased the expressions of inflammatory cytokines TNF-alpha, ICAM-1, and 
      complement C3a receptor (C3aR). We also noticed the increased phosphorylation of 
      ERK 1/2 in bEND.3 cells in OGD group. AKBA treatment significantly attenuated 
      expression levels of these inflammatory proteins and prevented the degradation of 
      ZO-1 and Occludin following OGD. In conclusion, AKBA treatment provides 
      protection against endothelial cell dysfunction following OGD by attenuating 
      oxidative stress and inflammation.
FAU - Ahmad, Saif
AU  - Ahmad S
AUID- ORCID: 0000-0003-2410-574X
AD  - Department of Neurosurgery, Barrow Neurological Institute, St. Joseph's Hospital 
      and Medical Center (SJHMC), Dignity Health, 350 W Thomas Rd, Phoenix, AZ, 85013, 
      USA. saif.ahmad@barrowneuro.org.
FAU - Khan, Shah Alam
AU  - Khan SA
AD  - Department of Neurosurgery, Barrow Neurological Institute, St. Joseph's Hospital 
      and Medical Center (SJHMC), Dignity Health, 350 W Thomas Rd, Phoenix, AZ, 85013, 
      USA.
AD  - Department of Pharmacy, Oman Medical College, Postal Code 130, Muscat, Sultanate 
      of Oman.
FAU - Kindelin, Adam
AU  - Kindelin A
AD  - Department of Neurosurgery, Barrow Neurological Institute, St. Joseph's Hospital 
      and Medical Center (SJHMC), Dignity Health, 350 W Thomas Rd, Phoenix, AZ, 85013, 
      USA.
FAU - Mohseni, Tasha
AU  - Mohseni T
AD  - Department of Neurosurgery, Barrow Neurological Institute, St. Joseph's Hospital 
      and Medical Center (SJHMC), Dignity Health, 350 W Thomas Rd, Phoenix, AZ, 85013, 
      USA.
FAU - Bhatia, Kanchan
AU  - Bhatia K
AD  - Department of Neurosurgery, Barrow Neurological Institute, St. Joseph's Hospital 
      and Medical Center (SJHMC), Dignity Health, 350 W Thomas Rd, Phoenix, AZ, 85013, 
      USA.
FAU - Hoda, Md Nasrul
AU  - Hoda MN
AD  - Department of Neurology, Barrow Neurological Institute, St. Joseph's Hospital and 
      Medical Center (SJHMC), Dignity Health, Phoenix, AZ, 85013, USA.
AD  - Department of Neurobiology, Barrow Neurological Institute, St. Joseph's Hospital 
      and Medical Center (SJHMC), Dignity Health, Phoenix, AZ, 85013, USA.
FAU - Ducruet, Andrew F
AU  - Ducruet AF
AD  - Department of Neurosurgery, Barrow Neurological Institute, St. Joseph's Hospital 
      and Medical Center (SJHMC), Dignity Health, 350 W Thomas Rd, Phoenix, AZ, 85013, 
      USA. andrew.ducruet@barrowbrainandspine.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190912
PL  - United States
TA  - Neuromolecular Med
JT  - Neuromolecular medicine
JID - 101135365
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Antioxidants)
RN  - 0 (Complement Inactivating Agents)
RN  - 0 (Plant Extracts)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Triterpenes)
RN  - 0 (acetyl-11-ketoboswellic acid)
RN  - IY9XDZ35W2 (Glucose)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Antioxidants/*pharmacology
MH  - Apoptosis/*drug effects
MH  - Boswellia/*chemistry
MH  - Cell Hypoxia
MH  - Complement Activation/*drug effects
MH  - Complement Inactivating Agents/*pharmacology
MH  - DNA Damage
MH  - Endothelial Cells/cytology/*drug effects/metabolism
MH  - Glucose/pharmacology
MH  - Hypoxia-Ischemia, Brain/*metabolism
MH  - Inflammation
MH  - MAP Kinase Signaling System/drug effects
MH  - Mice
MH  - Oxidative Stress/*drug effects
MH  - Oxygen/pharmacology
MH  - Plant Extracts/chemistry
MH  - Plants, Medicinal/*chemistry
MH  - Reactive Oxygen Species/analysis
MH  - Triterpenes/*pharmacology
OTO - NOTNLM
OT  - AKBA
OT  - BBB
OT  - Complement C3a receptor
OT  - Inflammation
OT  - OGD
OT  - bEND.3
EDAT- 2019/09/14 06:00
MHDA- 2021/02/02 06:00
CRDT- 2019/09/14 06:00
PHST- 2019/06/15 00:00 [received]
PHST- 2019/09/04 00:00 [accepted]
PHST- 2019/09/14 06:00 [pubmed]
PHST- 2021/02/02 06:00 [medline]
PHST- 2019/09/14 06:00 [entrez]
AID - 10.1007/s12017-019-08569-z [pii]
AID - 10.1007/s12017-019-08569-z [doi]
PST - ppublish
SO  - Neuromolecular Med. 2019 Dec;21(4):505-516. doi: 10.1007/s12017-019-08569-z. Epub 
      2019 Sep 12.