Expression of NLRP3 inflammasome in BALB/c mice with imiquimod-induced psoriasis-like inflammation and therapeutic effect of mustard seed (Sinapis Alba Linn).
- Author:
Jian HU
1
;
Runping YANG
;
Chunmiao WEN
;
Hengjin LI
;
Hua ZHAO
Author Information
- Publication Type:Journal Article
- MeSH: Aminoquinolines; adverse effects; Animals; Carrier Proteins; metabolism; Caspase 1; metabolism; Female; Inflammasomes; metabolism; Inflammation; drug therapy; pathology; Interleukin-18; metabolism; Interleukin-1beta; metabolism; Mice; Mice, Inbred BALB C; Mustard Plant; chemistry; NLR Family, Pyrin Domain-Containing 3 Protein; Phytotherapy; Psoriasis; chemically induced; drug therapy; metabolism; Seeds; chemistry
- From: Journal of Southern Medical University 2013;33(9):1394-1398
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of NLRP3 inflammasome in imiquimod-induced psoriasis-like inflammation in mice and the therapeutic effects of mustard seed (Sinapis Alba Linn).
METHODSThirty BALB/c mice were randomized equally into blank control group (fed with normal forage and treated with vehicle), model group (fed with normal forage and treated with 5% imiquimod cream), and experimental group (fed with 5% mustard seed forage and treated with 5% imiquimod cream). RT-PCR was used to detect the mRNA expression of NLRP3, ASC, caspase-1, and caspase-11. Immunohistochemistry was performed to determine the expression and distribution of ASC and caspase-1. ELISA was used to test the serum levels of interleukin-1β (IL-1β) and IL-18.
RESULTSCompared with the blank control group, the mice with imiquimod-induced psoriasis-like inflammation showed significantly increased NLRP3, ASC, caspase-1, and caspase-11 mRNA expressions, ASC and caspase-1 protein expressions , and serum levels of IL-1β and IL-18 (P<0.05). These changes were obviously attenuated by feeding the mice with mustard seed.
CONCLUSIONNLRP3 inflammasome is involved in imiquimod-induced psoriasis-like inflammation in mice, and mustard seed may suppress the inflammation induced by IL-1β and IL-18 through down-regulating the expression of NLRP3 inflammasome.