Fig 1: Schematic diagram of the proposed mechanism of amyloid β1-40 oligomer-induced ARPE-19 cell damage and LBP’s effects by anti-Aβ1-40 oligomerization and anti-pyroptosis. (A) In ARPE-19 cells, Aβ1-40 oligomers activate the NLRP3 inflammasome (NLRP3, the adaptor ASC, and pro-caspase-1), which subsequently leads to the generation of caspase-1. Caspase-1 cleaves Pro-IL-1β and Pro-IL-18, yielding IL-1β and IL-18, respectively. At the same time, C-GSDMD-N is also cleaved by caspase-1 thereby generating GSDMD-N and GSDMD-C. GSDMD-N moves to the cell membrane and forms ‘‘pores’’, allowing the newly generated IL-1β and IL-18 to be released from the cell. (B) Lycium barbarum polysaccharide (LBP) inhibits Aβ1-40 oligomerization and reverses the activation of pyroptosis, thereby protecting ARPE-19 cells from Aβ1-40 oligomers-induced cell death.
Fig 2: Changes in plasma cytokine levels and QICI values before (pre) and after (post) oral intake of (A) Lactobacillus plantarum SNK12 and (B) Bifidobacterium longum BB536. QICI was defined as follows: QICI=(TNF-α) x (IL-1β) x (IL-18) x (IL-8)/(IL-6), where brackets represent the plasma level of the cytokine in pg/ml. Cross marks denote outliers. Each red line represents the change of the medians. The data were statistically analyzed using the Friedman test followed by the Nemenyi post hoc test. QICI, Qingfei Paidu decoction-induced innate cytokine index.
Fig 3: IL-18 in serum samples as found in quantitative IL-18 ELISA. Quantitative IL-18 ELISA was done as per manufacturer’s instructions. “(+)” and “(−)” signs represent the presence and absence of microbes-Leishmaina donovani (LD), Leptomonas seymouri narna like virus 1 (Lepsey NLV1). VL- Visceral Leishmania, PKDL-Post Kala-azar Dermal Leishmaniasis. ‘p’ values were calculated from actual IL-18 concentration in three replicates for each serum sample, by two tailed, unpaired t test at 95% level of significance. (*p = 0.002, **p = 0.0126).
Fig 4: Hsa_circ_0010957 depletion blocks IL-6 induced activation of STAT3 signaling. (A) STAT3 and phosphorylated STAT3 protein levels when CD4+ T cells were treated with IL-6 and transfected with hsa_circ_0010957 siRNA and miR-125b inhibitor. (B-D) IL-18, IL-6 and IL-17 levels detected in cell supernatant when CD4+ T cells were treated with IL-6 and transfected with hsa_circ_0010957 siRNA and miR-125b inhibitor. Data are shown as mean ± SD *P<0.05. NS, no significance; IL, interleukin; miR, microRNA; siRNA, small interfering RNA; NC, negative control.
Fig 5: Hsa_circ_0010957 modulates inflammatory cytokines secretion via miR-125b. (A) Overexpression or silencing efficiency of hsa_circ_0010957 or miR-125b in CD4+ T cells of SLE detected by reverse transcription-quantitative PCR. (B-D) IL-18, IL-6 and IL-17 levels detected in cell supernatant after CD4+ T cells were transfected with hsa_circ_0010957 siRNAs and miR-125b inhibitor. (E-J) Pearson's correlation analysis between hsa_circ_0010957 or miR-125b expressions in CD4+ T cells of SLE with inflammatory cytokines in serum of patients with SLE. Data are shown as mean ± SD *P<0.05. SLE, systemic lupus erythematosus; miR, microRNA; siRNA, small interfering RNA; NC, negative control; IL, interleukin.
Supplier Page from Abcam for Human IL-18 ELISA Kit