ArticleMolecular neurobiology2018
Role of 3-Acetyl-11-Keto-Beta-Boswellic Acid in Counteracting LPS-Induced Neuroinflammation via Modulation of miRNA-155.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 52 citations in OpenAlex.
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- Modulation of Redox Balance by Phytochemicals: Implications for Cardiovascular Health.Nutrients · 2026Review
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- Unphosphorylated STAT1 binds to the BST2 transcription promoter, promoting increased AKBA anchoring on HPMECs to alleviate ARDS.Scientific reports · 2025Article
- Role of Decreased Expression of miR-155 and miR-146a in Peripheral Blood of Type 2 Diabetes Mellitus Patients with Diabetic Peripheral Neuropathy [Letter].Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Mitigating Traumatic Brain Injury: A Narrative Review of Supplementation and Dietary Protocols.Nutrients · 2024Review
- Dietary curcumin supplementation enhances growth performance and anti-inflammatory functions by modulating gut microbiota, microbiota-derived metabolites, and expression of inflammation-related genes in broilers.Journal of animal science · 2024Article
- Protective Mechanisms of 3-Acetyl-11-keto-β-Boswellic Acid and Piperine in Fluid Percussion Rat Model of Traumatic Brain Injury Targeting Nrf2 and NFkB Signaling.Neurotoxicity research · 2023Article
- Knockdown of SEMA7A alleviates MPPImmunity, inflammation and disease · 2023Article
- Preventive effects of arctigenin from Arctium lappa L against LPS-induced neuroinflammation and cognitive impairments in mice.Metabolic brain disease · 2022Article
- Article
- Novel Nutraceutical Compounds in Alzheimer Prevention.Biomolecules · 2022Review
- Nrf2/HO-1 Signaling Activator Acetyl-11-keto-beta Boswellic Acid (AKBA)-Mediated Neuroprotection in Methyl Mercury-Induced Experimental Model of ALS.Neurochemical research · 2021Article
- TLR4 signaling in the development of colitis-associated cancer and its possible interplay with microRNA-155.Cell communication and signaling : CCS · 2021Review
- Opposite effects of miR-155 in the initial and later stages of lipopolysaccharide (LPS)-induced inflammatory response.Journal of Zhejiang University. Science. B · 2021Article
- Alogliptin Attenuates Lipopolysaccharide-Induced Neuroinflammation in Mice Through Modulation of TLR4/MYD88/NF-κB and miRNA-155/SOCS-1 Signaling Pathways.The international journal of neuropsychopharmacology · 2021Article
- The Anti-Inflammatory Properties of Phytochemicals and Their Effects on Epigenetic Mechanisms Involved in TLR4/NF-κB-Mediated Inflammation.Frontiers in immunology · 2021Review
- GenusIranian journal of basic medical sciences · 2020Review
- Evaluation of Anti-inflammatory Nutraceuticals in LPS-induced Mouse Neuroinflammation Model: An Update.Current neuropharmacology · 2020Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroinflammation is one of the most important mechanisms underlying neurodegeneration. Lipopolysaccharide (LPS) is a potent inflammogen which causes cognitive dysfunction. Boswellia serrata is known since many years as a powerful anti-inflammatory herbal drug. Its beneficial effect mainly arises from inhibition of 5-lipoxygenase (5-LO) enzyme. 3-acetyl-11-keto-β-boswellic acid (AKBA) is the most potent 5-LO inhibitor extracted from the oleo-gum-resin of Boswellia serrata. The aim of the present work is to study the molecular mechanisms underlying the anti-inflammatory and neuroprotective effects of AKBA and dexamethasone (DEX) in LPS-induced neuroinflammatory model. A single intraperitoneal (i.p.) dose of LPS (0.8 mg/kg) was injected to induce cognitive dysfunction. The LPS-treated mice were administered for 7 days with either AKBA or DEX at intraperitoneal doses of 5 and 1 mg/kg, respectively. Cognitive, locomotor functions, and anxiety level were first examined. The level of the phosphorylated inhibitory protein for NF-κB, IκB-α (P-IκB-α), was measured, and the expression levels of the inflammatory microRNA-155 (miR-155) and its target gene, suppressor of cytokine signaling-1 (SOCS-1), were determined in the brain. Moreover, the level of carbonyl proteins as a measure of oxidative stress and several cytokines as well as markers for apoptosis and amyloidogenesis was detected. Results showed that AKBA and DEX reversed the behavioral dysfunction induced by LPS. AKBA decreased P-IκB-α, miRNA-155 expression level, and carbonyl protein content. It restored normal cytokine level and increased SOCS-1 expression level. It also showed anti-apoptotic and anti-amyloidogenic effects in LPS-injected mice. These findings suggest AKBA as a therapeutic drug for alleviating the symptoms of neuroinflammatory disorders.
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