Title of article :
Malaysian brown macroalgaPadina australis mitigates lipopolysaccharide-stimulated neuroinflammation in BV2 microglial cells
Author/Authors :
Subermaniam ، Kogilavani Department of Anatomy - Faculty of Medicine - Universiti Malaya , Lew ، Sze Yuen Department of Anatomy - Faculty of Medicine - Universiti Malaya , Yow ، Yoon Department of Biological Sciences - School of Medical and Life Sciences - Sunway University , Lim ، Siew Huah Department of Chemistry - Faculty of Science - Universiti Malaya , Yu ، Wing Shan Neuromodulation Laboratory - School of Biomedical Sciences, Li Ka Shing Faculty of Medicine - University of Hong Kong , Lim ، Lee Wei Neuromodulation Laboratory - School of Biomedical Sciences, Li Ka Shing Faculty of Medicine - University of Hong Kong , Wong ، Kah Hui Department of Anatomy - Faculty of Medicine - Universiti Malaya
Abstract :
Objective(s): Neuroinflammation and microglial activation are pathological features in central nervous system disorders. Excess levels of reactive oxygen species (ROS) and pro-inflammatory cytokines have been implicated in exacerbation of neuronal damage during chronic activation of microglial cells. Padina australis, a brown macroalga, has been demonstrated to have various pharmacological properties such as anti-neuroinflammatory activity. However, the underlying mechanism mediating the anti-neuroinflammatory potential of P. australis remains poorly understood. We explored the use of Malaysian P. australis in attenuating lipopolysaccharide (LPS)-stimulated neuroinflammation in BV2 microglial cells. Materials and Methods: Fresh specimens of P. australis were freeze-dried and subjected to ethanol extraction. The ethanol extract (PAEE) was evaluated for its protective effects against 1 µg/ml LPS-stimulated neuroinflammation in BV2 microglial cells. Results: LPS reduced the viability of BV2 microglia cells and increased the levels of nitric oxide (NO), prostaglandin E2 (PGE2), intracellular reactive oxygen species (ROS), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6). However, the neuroinflammatory response was reversed by 0.5–2.0 mg/ml PAEE in a dose-dependent manner. Analysis of liquid chromatography-mass spectrometry (LC-MS) of PAEE subfractions revealed five compounds; methyl α-eleostearate, ethyl α-eleostearate, niacinamide, stearamide, and linoleic acid. Conclusion: The protective effects of PAEE against LPS-stimulated neuroinflammation in BV2 microglial cells were found to be mediated by the suppression of excess levels of intracellular ROS and pro-inflammatory mediators and cytokines, denoting the protective role of P. australis in combating continuous neuroinflammation. Our findings support the use of P. australis as a possible therapeutic for neuroinflammatory and neurodegenerative diseases.
Keywords :
Brown algae , BV2 microglial , Cytokines , Major compounds , Neuroinflammation , Oxidative Damage
Journal title :
Iranian Journal of Basic Medical Sciences
Journal title :
Iranian Journal of Basic Medical Sciences