ArticleNeuromolecular medicine2019
Acetyl-11-keto-β-boswellic acid (AKBA) Attenuates Oxidative Stress, Inflammation, Complement Activation and Cell Death in Brain Endothelial Cells Following OGD/Reperfusion.
Article in Neuromolecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 48 citations in OpenAlex.
- Article
- 3-Acetyl-11-Keto-β-Boswellic acid (AKBA) Attenuated 6-Hydroxydopamine (6-OHDA)-Induced Toxicity in SH-SY5Y Cells via Modulation of Akt/mTOR Pathway.Molecular neurobiology · 2025Article
- Multidimensional analysis of cerebral iron and vascular changes in chronic unilateral middle cerebral artery stenosis with quantitative susceptibility mapping, arterial spin labeling and high-resolution vessel wall imaging-a pilot study.Quantitative imaging in medicine and surgery · 2025Article
- Acetyl 11-Keto Beta-Boswellic Acid Improves Neurological Functions in a Mouse Model of Multiple Sclerosis.Inflammation · 2025Article
- Article
- Endothelial Dysfunctions in Blood-Brain Barrier Breakdown in Alzheimer's Disease: From Mechanisms to Potential Therapies.CNS neuroscience & therapeutics · 2024Review
- The effects of olibanum on male reproductive system damage in a lipopolysaccharide induced systemic inflammation model in rat.Heliyon · 2024Article
- Activation of SIRT1/Nrf2/HO-1 and Beclin-1/AMPK/mTOR autophagy pathways by eprosartan ameliorates testicular dysfunction induced by testicular torsion in rats.Scientific reports · 2024Article
- Activation of testosterone-androgen receptor mediates cerebrovascular protection by photobiomodulation treatment in photothrombosis-induced stroke rats.CNS neuroscience & therapeutics · 2024Article
- Exploration of the mechanism of Taohong Siwu Decoction for the treatment of ischemic stroke based on CCL2/CCR2 axis.Frontiers in pharmacology · 2024Article
- MicroRNA-199a-5p attenuates blood-brain barrier disruption following ischemic stroke by regulating PI3K/Akt signaling pathway.PloS one · 2024Article
- Exploring the Anticancer Potential ofPlants (Basel, Switzerland) · 2023Article
- Caveolin-1 accelerates hypoxia-induced endothelial dysfunction in high-altitude cerebral edema.Cell communication and signaling : CCS · 2022Article
- Acetyl-11-Keto-Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Acetyl-11-Keto-Beta Boswellic Acid (AKBA) Protects Lens Epithelial Cells Against HFrontiers in pharmacology · 2022Article
- Pathophysiology of blood brain barrier dysfunction during chronic cerebral hypoperfusion in vascular cognitive impairment.Theranostics · 2022Review
- Article
- Boswellic acids/Boswellia serrata extract as a potential COVID-19 therapeutic agent in the elderly.Inflammopharmacology · 2021Review
- Apelin-36 Protects HT22 Cells Against Oxygen-Glucose Deprivation/Reperfusion-Induced Oxidative Stress and Mitochondrial Dysfunction by Promoting SIRT1-Mediated PINK1/Parkin-Dependent Mitophagy.Neurotoxicity research · 2021Article
- Facial nerve regeneration using silicone conduits filled with ammonia-functionalized graphene oxide and frankincense-embedded hydrogel.Inflammation and regeneration · 2021Article
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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-β-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-α, 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.
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