ssRNA40 sodium

ssRNA40 sodium (3 ng/μL; 3 h) downregulates the mRNA expression level of TLR2, upregulates the mRNA expression levels of TLR7, TLR8, RIG-I and MDA5, but has no effect on the mRNA expression level of TLR4 in purified human neutrophils^[1].
Co-administration of ssRNA40 sodium (3 ng/μL; 3 h) with TLR agonists significantly upregulates the mRNA expression of TLR2, TLR4, TLR7, TLR8, RIG-I and MDA5 in purified human neutrophils from healthy donors in a TLR agonist-dependent manner^[1].
ssRNA40 sodium (3 ng/μL; 8 h) significantly reduces the expression level of CD62L, promotes the secretion of IL-6 and TNF-α, and increases the production of ROS in purified human neutrophils, whereas it exerts no significant effect on the expression of CD11b^[1].
ssRNA40 sodium (0-20 μg/mL; 0-6 days) induces dose-dependent and time-dependent cell death in primary cortical neurons from wild-type mice in a TLR7-dependent, cell-autonomous, and MyD88-dependent manner (treatment with 10 μg/mL for 4 days reduces cell viability by approximately 30%), whereas primary cortical neurons from TLR7-knockout mice are completely protected^[2].
ssRNA40 sodium (10 μg/mL; 36 h) induces cell death in N1E-115 mouse neuroblastoma cells^[2].
ssRNA40 sodium (10 μg/mL; 3 days) activates caspase-3 in primary mouse cortical neurons, and inhibition of caspase-3 blocks ssRNA40-induced neuronal cell death^[2].
ssRNA40 sodium (1-25 μg/mL; 6-24 h) induces dose-dependent and time-dependent secretion of TNF-α, IL-6, MCP-1 and RANTES (but not IL-10) from primary microglia of wild-type mice in a TLR7-dependent manner, whereas primary microglia from TLR7-knockout mice do not secrete these cytokines upon ssRNA40 stimulation^[2].
ssRNA40 sodium (2 μg/mL; 1-24 h) activates the TLR8/IRE1α-XBP1 pathway in human MDDCs, induces XBP1 splicing and sXBP1 promoter binding, and significantly promotes the expression of proinflammatory cytokines (IL-1β, IL-6, TNFα) at both mRNA and protein levels, with all these effects dependent on the activities of TLR8 and IRE1α^[3].
ssRNA40 sodium (6 h) activates CD3⁻CD56⁺/⁻ NK cells in HIV-1-negative peripheral blood mononuclear cells (PBMCs); when ssRNA40 is complexed with Dotap, the activation effect is significantly enhanced, with the median percentage of CD69⁺ NK cells reaching 28.8% after 6 h of stimulation^[4].
ssRNA40 sodium (5 μg/mL; 24-48 h) activates the NLRP3 inflammasome in human primary monocyte-derived microglia (HMG), induces the substantial expression and secretion of pro-inflammatory cytokines (IL-1β, IL-18) and neurotoxic cytokines (C1q, IL-1α, TNF-α), and the release of IL-1β depends on the activities of NLRP3 and caspase-1^[5].
Supernatant from HMG activated by ssRNA40 sodium (5 μg/mL; 48 h) induces significant neurotoxicity in human primary neurons (HPN), including reduced cell viability and neurite damage^[5].
ssRNA40 sodium (5 μg/mL; 24 h) induces NLRP3-dependent mitochondrial damage in HMG, including increased ROS production and loss of mitochondrial membrane potential^[5].
ssRNA40 sodium (5 μg/mL; 24 h) upregulates the expression of autophagy/mitophagy receptors (SQSTM1, OPTN, PINK1, Parkin) and induces their mitochondrial recruitment in HMG and HFMG^[5].
ssRNA40 sodium (5 μg/mL; 24-48 h) impairs autophagic flux in HMG, which in turn leads to persistent activation of the NLRP3 inflammasome, activation of caspase-1, and pyroptosis^[5].
ssRNA40 sodium (2 μg/mL; 16 h) induces robust IFN-α production in primary human plasmacytoid dendritic cells (pDC), and this response is significantly dependent on the TLR7 signaling pathway and autophagy; inhibition of either pathway drastically reduces IFN-α secretion^[6].
ssRNA40 sodium (2 μg/mL; 16 h) upregulates the expression of autophagy-related proteins (ATG7 and LC3-II) and induces the formation of a large number of autophagosomes in primary human pDCs^[6].
ssRNA40 sodium (2 μg/mL; 12 h) induces IRF7 activation (nuclear translocation and phosphorylation) in primary human pDCs and promotes the co-expression of activated IRF7 with autophagic LC3B puncta; inhibition of autophagy or the mTOR signaling pathway attenuates this activation^[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.