Salidroside Reduces Inflammation and Brain Injury After Permanent Middle Cerebral Artery Occlusion in Rats by Regulating PI3K/PKB/Nrf2/NFκB Signaling Rather than Complement C3 Activity.
Salidroside, the active constituents of Rhodiola rosea, is nervous after a while the middle cerebral artery occlusion (tMCAO). However, the impact in other experimental models of stroke are poorly understood. Here, we examined the effects of daily intraperitoneal injections salidroside in rats after permanent MCAO (pMCAO). the volume of cerebral infarction in 1 day after pMCAO was significantly reduced by treatment with 100 mg / kg / day salidroside, but not at 25 or 50 mg / kg / day, and benefits from salidroside increased significantly for at least 7 days of treatment, when it also accompanied by neurologic deficit score decreased.
These observations prompted us to investigate the underlying mechanisms of action salidroside. 100 mg / kg for 1 day salidroside increased Neun, Nrf2 and HO-1 downstream mediator, while reducing NF nuclear p50, IL-6, and TNF. Brusatol, Nrf2 inhibitor, blocked the action salidroside on Nrf2, NF p50, IL-6, and TNF.
Salidroside also increase the ratio of p-PKB / PKB at 1 day after pMCAO even before brusatol. LY294002, PI3K inhibitors, to prevent these effects from salidroside, including those in Neun, p-PKB / PKB, Nrf2, HO-1, and pro-inflammatory mediators. Instead, salidroside no significant effect on brain levels of complement C3 after pMCAO, or on C3 activity as measured by the expression of cerebral Egr1.
Therefore, our findings suggest that salidroside reduce neuroinflammation and neuronal damage by regulating the PI3K / PKB / Nrf2 / NF signaling pathways after pMCAO, and that this neuroprotective effect does not involve modulation of complement C3 activity.
Salidroside Reduces Inflammation and Brain Injury After Permanent Middle Cerebral Artery Occlusion in Rats by Regulating PI3K/PKB/Nrf2/NFκB Signaling Rather than Complement C3 Activity.
Identification of the canonical NF (C-NF) pathway in uveal melanoma and its relation to patient outcomes.
Inflammation of the uveal melanoma (UM) associated with a poor prognosis. This is a rare type of cancer, in which the metastasis is usually fatal within a year. Infiltration with inflammatory infiltration rise to the development of the disease but does not seem to inhibit metastasis. The Canonical NF (C-NF) pathway is known to play an important role in tumor inflammation.
Therefore we, studying the canonical NF protein expression and their prognostic relevance in UM. Our study evaluated the expression of the protein C-NF (p65, p50 and c-Rel) using immunohistochemistry on sections of formalin-fixed 75 MW. Activation of NF subunit is determined on fresh tumor specimens by measuring the activity of DNA-binding core using ELISA NF test. Real-time PCR was performed on frozen matter on 58 tumor. The presence of heterodimers original C-NF (p65 / p50 and c-Rel / p50) was confirmed by co-immunoprecipitation followed by Western blotting.
We observed a high nuclear immunoreactivity of p65, p50 and c-Rel protein in 54, 60 and 41% of cases MW, respectively. C-NF protein expression significantly correlated with environmental parameters associated with inflammation of the UM. Nuclear immunoreactivity of p65 and p50 was associated with lower patient survival (p = 0.041; p = 0.048), whereas c-Rel are not. Our findings suggest that protein C-NF expressed more often in UM with inflammation than those without inflammation. Activation of NF canonical pathway more often in high-risk patients with UM.
Description: A polyclonal antibody for NFkB p65 from Human | Mouse | Rat. The antibody is produced in rabbit after immunization with Human A synthesized peptide derived from human NF-kappaB p65. The Antibody is tested and validated for WB, IHC, ICC/IF, IP assays with the following recommended dilutions: WB (1:2000), IHC (1:200), ICC/IF (1:200). This NFkB p65 antibody is unconjugated.
Description: A polyclonal antibody for NFkB p65 from Human | Mouse | Rat. The antibody is produced in rabbit after immunization with Human A synthesized peptide derived from human NF-kappaB p65. The Antibody is tested and validated for WB, IHC, ICC/IF, IP assays with the following recommended dilutions: WB (1:2000), IHC (1:200), ICC/IF (1:200). This NFkB p65 antibody is conjugated to ATTO 390.
Description: A polyclonal antibody for NFkB p65 from Human | Mouse | Rat. The antibody is produced in rabbit after immunization with Human A synthesized peptide derived from human NF-kappaB p65. The Antibody is tested and validated for WB, IHC, ICC/IF, IP assays with the following recommended dilutions: WB (1:2000), IHC (1:200), ICC/IF (1:200). This NFkB p65 antibody is conjugated to ATTO 488.
Description: A polyclonal antibody for NFkB p65 from Human | Mouse | Rat. The antibody is produced in rabbit after immunization with Human A synthesized peptide derived from human NF-kappaB p65. The Antibody is tested and validated for WB, IHC, ICC/IF, IP assays with the following recommended dilutions: WB (1:2000), IHC (1:200), ICC/IF (1:200). This NFkB p65 antibody is conjugated to ATTO 594.
Description: A polyclonal antibody for NFkB p65 from Human | Mouse | Rat. The antibody is produced in rabbit after immunization with Human A synthesized peptide derived from human NF-kappaB p65. The Antibody is tested and validated for WB, IHC, ICC/IF, IP assays with the following recommended dilutions: WB (1:2000), IHC (1:200), ICC/IF (1:200). This NFkB p65 antibody is conjugated to Biotin.
Description: A polyclonal antibody for NFkB p65 from Human | Mouse | Rat. The antibody is produced in rabbit after immunization with Human A synthesized peptide derived from human NF-kappaB p65. The Antibody is tested and validated for WB, IHC, ICC/IF, IP assays with the following recommended dilutions: WB (1:2000), IHC (1:200), ICC/IF (1:200). This NFkB p65 antibody is conjugated to FITC.
This observation may help to understand the behavior of high-risk tumors, the upregulation of the protein C-NF NF contributes to tumor aggressiveness.The RELA members of family of transcription factors, p50, and cRel form of homo and heterodimers are inhibited by IκBα, IκBβ, and IκBε. NF members of this family have diverse biological functions, and they are different expression profiles, leading to different concentrations in different tissue types.
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