Abstract
BackgroundExcessive production of inflammatory mediators such as nitric oxide (NO) and proinflammatory cytokines like tumour necrosis factor-alpha (TNF-α) from activated microglia contributes to uncontrolled inflammation in neurodegenerative diseases. This study investigated the protective role of five endophytic extracts (HAB16R12, HAB16R13, HAB16R14, HAB16R18 and HAB8R24) against LPS-induced inflammatory events in vitro. These endophytic extracts were previously found to exhibit potent neuroprotective effect against LPS-challenged microglial cells.MethodsThe effects of these fungal endophytic extracts against nitric oxide (NO), CD40 phenotype and, pro- and anti-inflammatory cytokine production in lipopolysaccharide (LPS)-stimulated BV2 microglia cells were examined using commercially available assay kits, immunophenotyping and flow cytometry, respectively.ResultsMicroglia pre-treated with the five endophytic extracts (0.1 mg/mL) reduced NO production without compromising cell viability. Whilst CD40 expression in LPS-stimulated microglia was not significantly different with or without the influence of endophytic extracts, expression of the proinflammatory cytokines, IL-6 and TNF-α in LPS-stimulated microglia was significantly (P < 0.05) inhibited by these endophytic extracts.ConclusionsThe outcomes suggest that the neuroprotective effect of the fungal endophytic extracts is likely mediated through supression of neuroinflammation. To our knowledge, this is the first report of the effect of a fungal endophytic extract in controlling inflammation in BV2 microglia cells.Electronic supplementary materialThe online version of this article (doi:10.1186/s12906-015-0685-5) contains supplementary material, which is available to authorized users.
Highlights
Excessive production of inflammatory mediators such as nitric oxide (NO) and proinflammatory cytokines like tumour necrosis factor-alpha (TNF-α) from activated microglia contributes to uncontrolled inflammation in neurodegenerative diseases
The present study found the NO lowering effect of pre-treatment with endophytic extracts (0.1–1 mg/mL) to be either comparable to or otherwise better than that of standard nitric oxide synthase (NOS) inhibitor, L-NAME
It is noteworthy that the protective effects of pre-treatment with endophytic extracts as observed had no effect on basal NO release by microglia (Additional file 1: Figure S1)
Summary
Excessive production of inflammatory mediators such as nitric oxide (NO) and proinflammatory cytokines like tumour necrosis factor-alpha (TNF-α) from activated microglia contributes to uncontrolled inflammation in neurodegenerative diseases. Microglia account for approximately 12 % of cell population [4] in the central nervous system (CNS) They are brain-specific macrophages that provide trophic support and maintains homeostasis in healthy tissue [5]. During brain infection or injury, microglia become activated and up-regulate a variety of surface receptors which include the major histocompatibility complex and complement receptors [1]. They release various pro-survival neurotrophic factors like brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) and nerve growth factor (NGF) [6], and proinflammatory molecules such as tumour necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β) and free radicals nitric oxide (NO) and superoxide
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