ABSTRACT
Immune thrombocytopenia (ITP) is an autoimmune disease mediated by acquired immunity, with platelets decreased and hemorrhage being the primary clinical manifestations. The responses and platelet count levels after early treatment are important factors affecting long-term prognosis, however, current diagnostic methods and disease evaluation approaches are limited, and lack of specific biomarkers. In recent years, various biomolecules have been proposed as potential biomarkers for ITP. This paper reviews the value and advances in ITP-related biomarkers.
ABSTRACT
Objective:To investigate the effect of sesamin on mast cell activation and its inflammatory mediator release,as well as its possible mechanisms of action.Methods:HCM-1 cells were activation by stimulation with 10 μg/ml anti-DNP IgE for 6 h and challenge with 100 ng/ml DNP-HAS for 10 min.Sesamin was administration at the concentration of 25,50 and 100 μg/L prior to DNP-HAS challenge,subsequently the effect of sesamin on mast cell degranulation was investigated by light microscope,and histamine release and expression of cytokines such as TNF-α IL-6,IL-1β,IL-8 of mast cells after sesamin treatment were investigated by ELISA.Western blot was used to determine the effect of sesamin on FcεRI downstream signaling including Lyn,Syk and PKCα activation,and IκBα phosphorylation and NF-κB activation.Results:DNP-HAS significantly increased mast cell degranulation,histamine release and those cytokines expression,enhanced Lyn,Syk,PKCα,IκBα phosphorylation and NF-κB activation(P<0.05). Sesamin(50,100 μg/L) significantly decreased mast cell degranulation,histamine release and cytokines expression (TNF-α,IL-4,IL-1β,and IL-8),reduced activity of Lyn,Syk,kinases and PKCα and IκBα phosphorylation,and inhibited NF-κB activation(P<0.05).Conclusion: Sesamin suppresses mast cell activation and inflammatory mediators release through inhibition of PKCα/NF-κB signaling pathway.
ABSTRACT
Fucoidan has been reported to exhibit various beneficial activities ranging from to antivirus and anticancer properties. However, little information is available about the effects of fucoidan on cerebral ischemia-reperfusion injury (IRI). Our study aimed to explore the effects of fucoidan on cerebral IRI, as well as the underlying mechanisms. Sprague-Dawley (SD) rats were randomly subjected to four groups: Sham, IRI+saline (IRI+S), IRI+80 mg/kg fucoidan (IRI+F80), and IRI+160 mg/kg fucoidan (IRI+F160). Fucoidan (80 mg/kg or 160 mg/kg) was intraperitoneally injected from 7 days before the rats were induced to cerebral IRI model with middle cerebral artery occlusion (MCAO) method. At 24 h after reperfusion, neurological deficits and the total infarct volume were determined. The levels of inflammation-associated cytokines (interleukin (IL)-1β, IL-6, myeloperoxidase (MPO), and tumor necrosis factor (TNF)-α), oxidative stress-related proteins (malondialdehyde (MDA) and superoxide dismutase (SOD)) in the ischemic brain were measured by enzyme-linked immunosorbent assay (ELISA). Besides, the levels of apoptosis-related proteins (p-53, Bax, and B-cell lymphoma (Bcl)-2) and mitogen-activated protein kinase (MAPK) pathway (phosphorylation-extracellular signal-regulated kinase (p-ERK), p-c-Jun N-terminal kinase (JNK), and p-p38) were measured. Results showed that administration of fucoidan significantly reduced the neurological deficits and infarct volume compared to the IRI+S group in a dose-dependent manner. Also, fucoidan statistically decreased the levels of inflammation-associated cytokines, and oxidative stress-related proteins, inhibited apoptosis, and suppressed the MAPK pathway. So, Fucoidan plays a protective role in cerebral IRI might be by inhibition of MAPK pathway.