Modulation of microglial functions by methyl jasmonate
Neuroinflammation contributes to the neurodegenerative processes in Alzheimer’s disease (AD); therefore, characterization of novel drug candidates aimed at combatting inflammation in the central nervous system is one of the potential avenues for the development of effective AD treatment and preventi...
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| Format: | Article |
| Language: | English |
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Wolters Kluwer Medknow Publications
2018-01-01
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| Series: | Neural Regeneration Research |
| Subjects: | |
| Online Access: | http://www.nrronline.org/article.asp?issn=1673-5374;year=2018;volume=13;issue=7;spage=1290;epage=1293;aulast=McKenzie |
| _version_ | 1818280262474137600 |
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| author | Jordan A McKenzie Andis Klegeris |
| author_facet | Jordan A McKenzie Andis Klegeris |
| author_sort | Jordan A McKenzie |
| collection | DOAJ |
| description | Neuroinflammation contributes to the neurodegenerative processes in Alzheimer’s disease (AD); therefore, characterization of novel drug candidates aimed at combatting inflammation in the central nervous system is one of the potential avenues for the development of effective AD treatment and prevention strategies. Non-neuronal microglial cells orchestrate neuroinflammatory reactions, and their adverse activation has been linked to AD pathogenesis. Methyl jasmonate (MJ) has anti-cancer properties and has also been shown to reduce peripheral inflammation in pre-clinical models. Recently, anti-neuroinflammatory activity of MJ was demonstrated in mice, but the exact cellular and molecular mechanisms responsible for this beneficial effect are unknown. We hypothesized that MJ can regulate select microglial functions, and used two different in vitro models of microglia to test this hypothesis. MJ inhibited the production of damaging reactive oxygen species by differentiated human HL-60 promyelocytic leukemia cells without reducing their viability. MJ also selectively upregulated phagocytic activity of murine BV-2 microglia, but had no effect on nitric oxide secretion by these cells. Since microglial phagocytosis can be beneficial for clearance of amyloid β aggregates in AD, the observed upregulation of phagocytic activity by MJ, combined with its inhibitory effect on reactive oxygen species production, supports continued studies of MJ as a candidate drug for managing adverse neuroinflammation in AD. |
| first_indexed | 2024-12-12T23:46:26Z |
| format | Article |
| id | doaj.art-d12215dea6c84bc3a1660800675824fd |
| institution | Directory Open Access Journal |
| issn | 1673-5374 |
| language | English |
| last_indexed | 2024-12-12T23:46:26Z |
| publishDate | 2018-01-01 |
| publisher | Wolters Kluwer Medknow Publications |
| record_format | Article |
| series | Neural Regeneration Research |
| spelling | doaj.art-d12215dea6c84bc3a1660800675824fd2022-12-22T00:06:51ZengWolters Kluwer Medknow PublicationsNeural Regeneration Research1673-53742018-01-011371290129310.4103/1673-5374.235078Modulation of microglial functions by methyl jasmonateJordan A McKenzieAndis KlegerisNeuroinflammation contributes to the neurodegenerative processes in Alzheimer’s disease (AD); therefore, characterization of novel drug candidates aimed at combatting inflammation in the central nervous system is one of the potential avenues for the development of effective AD treatment and prevention strategies. Non-neuronal microglial cells orchestrate neuroinflammatory reactions, and their adverse activation has been linked to AD pathogenesis. Methyl jasmonate (MJ) has anti-cancer properties and has also been shown to reduce peripheral inflammation in pre-clinical models. Recently, anti-neuroinflammatory activity of MJ was demonstrated in mice, but the exact cellular and molecular mechanisms responsible for this beneficial effect are unknown. We hypothesized that MJ can regulate select microglial functions, and used two different in vitro models of microglia to test this hypothesis. MJ inhibited the production of damaging reactive oxygen species by differentiated human HL-60 promyelocytic leukemia cells without reducing their viability. MJ also selectively upregulated phagocytic activity of murine BV-2 microglia, but had no effect on nitric oxide secretion by these cells. Since microglial phagocytosis can be beneficial for clearance of amyloid β aggregates in AD, the observed upregulation of phagocytic activity by MJ, combined with its inhibitory effect on reactive oxygen species production, supports continued studies of MJ as a candidate drug for managing adverse neuroinflammation in AD.http://www.nrronline.org/article.asp?issn=1673-5374;year=2018;volume=13;issue=7;spage=1290;epage=1293;aulast=McKenzieAlzheimer′s disease; anti-inflammatory; glia; neuroinflammation; neurodegeneration; neuroprotection; nitric oxide; phagocytosis; reactive nitrogen species; reactive oxygen species |
| spellingShingle | Jordan A McKenzie Andis Klegeris Modulation of microglial functions by methyl jasmonate Neural Regeneration Research Alzheimer′s disease; anti-inflammatory; glia; neuroinflammation; neurodegeneration; neuroprotection; nitric oxide; phagocytosis; reactive nitrogen species; reactive oxygen species |
| title | Modulation of microglial functions by methyl jasmonate |
| title_full | Modulation of microglial functions by methyl jasmonate |
| title_fullStr | Modulation of microglial functions by methyl jasmonate |
| title_full_unstemmed | Modulation of microglial functions by methyl jasmonate |
| title_short | Modulation of microglial functions by methyl jasmonate |
| title_sort | modulation of microglial functions by methyl jasmonate |
| topic | Alzheimer′s disease; anti-inflammatory; glia; neuroinflammation; neurodegeneration; neuroprotection; nitric oxide; phagocytosis; reactive nitrogen species; reactive oxygen species |
| url | http://www.nrronline.org/article.asp?issn=1673-5374;year=2018;volume=13;issue=7;spage=1290;epage=1293;aulast=McKenzie |
| work_keys_str_mv | AT jordanamckenzie modulationofmicroglialfunctionsbymethyljasmonate AT andisklegeris modulationofmicroglialfunctionsbymethyljasmonate |