Inflammatory damage plays a pivotal role in ischemic stroke pathogenesis and may represent one of the therapeutic targets. Z-Guggulsterone (Z-GS), an active component derived from myrrh, has been used to treat various diseases. The traditional uses suggest that myrrh is a good candidate for anti-inflammatory damage. This study was to investigate the anti-inflammatory and neuroprotective effects of Z-GS following cerebral ischemic injury, as well as the exact mechanisms behind them. Rat middle cerebral artery occlusion (MCAO) model and in vitro astrocytes oxygen-glucose deprivation (OGD) model were adopted to simulate ischemic stroke. Z-GS (30 or 60 mg/kg) was administered intraperitoneally immediately after reperfusion, while astrocytes were maintained in 30 or 60 μM Z-GS before OGD treatment. The results indicated that Z-GS significantly alleviated neurological deficits, infarct volume and histopathological damage in vivo, and increased the astrocytes viability in vitro. Moreover, the treatment of Z-GS inhibited the astrocytes activation and down-regulated the mRNA levels of pro-inflammatory cytokines. Furthermore, the activated TLR4-NF-κB signaling pathways induced by MCAO or OGD were significantly suppressed by Z-GS treatment, which was achieved via inhibiting the phosphorylation of JNK. Our results demonstrated that Z-GS exerted neuroprotective and anti-inflammatory properties through preventing activation of TLR4-mediated pathway in the activated astrocytes after ischemia injury. Therefore, Z-GS could be considered as a promising candidate for the treatment of ischemic stroke.
Pubmed ID: 30168601 RIS Download
Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.
This polyclonal targets TLR4
View all literature mentionsThis monoclonal targets GFAP (2E1)
View all literature mentionsThis monoclonal targets p-NFkappaB p65 (27.Ser 536)
View all literature mentionsThis monoclonal targets Genetic locus: RELA (human) mapping to 11q13.1; Rela (mouse) mapping to 19 A.
View all literature mentionsThis monoclonal targets p-IkappaB-alpha (Ser 32)
View all literature mentionsThis polyclonal targets Mapk9
View all literature mentionsThis monoclonal targets β-Actin
View all literature mentionsThis monoclonal targets JNK1 + JNK2 + JNK3(phospho T183+T183+T221) (phospho T183 + T183 + T221) antibody [EPR5693]
View all literature mentionsThis monoclonal targets Human NFKBIA
View all literature mentionsThis monoclonal targets β-Actin
View all literature mentionsThis monoclonal targets Human NFKBIA
View all literature mentionsThis monoclonal targets GFAP (2E1)
View all literature mentionsThis monoclonal targets JNK1 + JNK2 + JNK3(phospho T183+T183+T221) (phospho T183 + T183 + T221) antibody [EPR5693]
View all literature mentionsThis monoclonal targets p-NFkappaB p65 (27.Ser 536)
View all literature mentionsThis polyclonal targets TLR4
View all literature mentionsThis monoclonal targets p-IkappaB-alpha (Ser 32)
View all literature mentionsThis monoclonal targets Genetic locus: RELA (human) mapping to 11q13.1; Rela (mouse) mapping to 19 A.
View all literature mentionsThis polyclonal targets Mapk9
View all literature mentions