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Basic information of Nos2 :

Official Symbol of Gene Nos2
Species Mus musculus
Entrez Gene ID 18126
Official Full Name nitric oxide synthase 2, inducible
Also known as iNOS; Nos-2; Nos2a; i-NOS; NOS-II; MAC-NOS
Gene Type protein coding
dbXrefs Ensembl:ENSMUSG00000020826 AllianceGenome:MGI:97361
Map Location 11 B5; 11 46.74 cM

Sample information of multiple sclerosis:

Detected Sample brain
Sample Detail microglia
Detected Method Western blot analysis
Disease inflammatory effects
Disease subtype cerebral ischemia, multiple sclerosis, and Alzheimer’s disease
Population immortalized murine BV2 microglial cell
Sample Size N/A

Literature information of multiple sclerosis :

Pubmed ID 24244819
Year 2013
Title Kalopanaxsaponin A Exerts Anti-Inflammatory Effects in Lipopolysaccharide-Stimulated Microglia via Inhibition of JNK and NF-κB/AP-1 Pathways

Results of multiple sclerosis :

Expression up-regulation
Risk type Disease risk
Result we showed that kalopanaxsaponin A, a triterpenoid saponin isolated from Kalopanax pictus, inhibited inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and tumor necrosis factor (TNF)-α expression in lipopolysaccharide (LPS)-stimulated microglia, while kalopanaxsaponin A increased anti-infl ammatory cytokine interleukin (IL)-10 expression. Subsequent mechanistic studies revealed that kalopanaxsaponin A inhibited LPS-induced DNA binding activities of NF-κB and AP-1, and the phosphorylation of JNK without affecting other MAP kinases. Furthermore, kalopanaxsaponin A inhibited the intracellular ROS production with upregulation of anti-infl ammatory hemeoxygenase-1 (HO-1) expression. Based on the previous reports that JNK pathway is largely involved in iNOS and proinfl ammatory cytokine gene expression via modulating NF-κB/AP-1 and ROS, our data collectively suggest that inhibition of JNK pathway plays a key role in anti-infl ammatory effects of kalopanaxsaponin A in LPS-stimulated microglia
Mechanism/Pathway JNK pathway is largely involved in iNOS and proinfl ammatory cytokine gene expression via modulating NF-κB/AP-1 and ROS