Fig 1: Effect of EF on LPS-induced acute lung injury in mice.A: lungs from different groups were processed for histological evaluation 8 h after the LPS. B/D: The mRNA levels of TNFα and IL-6 were determined by quantitative real-time PCR. C/E: The BALF levels of TNF-α, IL-6 and IL-1β, determined by ELISA. #P<0.05, ##P<0.01 vs control; *P<0.05, **P<0.01 vs LPS.
Fig 2: NAC inhibits plasma inflammatory cytokine production in LDLR KO PM + HFD mice. There was a significant increase in TNF-α, IL-1β and IL-6 in LDLR KO HFD mice with or without PM compared with PM+ND or ND mice. NAC effectively inhibited inflammatory cytokine production. Inflammatory cytokines were also increased in mice with 1 week and 6 month HFD or PM + ND compared with ND mice. n=5-8. *P<0.01 vs. ND; **P<0.01 vs. HFD; #P<0.01 vs. PM + ND; ##P<0.01 vs. PM + HFD. ND, normal diet; HFD, high-fat diet; NAC, N-acetyl cysteine; PM, ambient fine particulate matter; LDLR, low-density lipoprotein receptor; KO, knockout.
Fig 3: Conclusion of this study. THC blocks P. a. LPS–induced oxidative responses by increasing Nrf2-HO-1 expression which attenuates the iNOS, COX-2, and p-NFκB expression. THC also inhibits the level of P. a. LPS–prompted JAK-STAT signaling and the inflammatory mediators IL-6, TNF-α, MIP-2, and IP-10 productions. Collectively, THC is a potent anti-inflammatory agent in brain encephalitis.
Fig 4: THC treatment reduces Snpp-prompted IP-10, IL-6, and nitrite production in P. a. LPS–stimulated BV2 microglial cells. BV2 microglial cells were pretreated with THC (40 μM) or HO-1 inhibitor Snpp (20 μM) for 1.5 h before being stimulated with P. aeruginosa LPS (0.1 μg/ml) for 24 h. The production of (a) IP-10, (b) IL-6, and (c) nitrite was determined using ELISA. The experimental quantitative data are presented in terms of mean ± SD (n = 3). Bars with the same letter represent no significant difference between the groups. Bars with different letters indicate a statistically significant (p < 0.05) difference between the groups.
Fig 5: STAT3/JAK blocker combined with THC reduces IL-6, TNF-α, MIP-2, IP-10, and nitrite production in P. a. LPS–stimulated BV2 microglial cells. BV2 microglial cells were pretreated with STAT3 inhibitor AG490 (15 μM), JAK inhibitor WP1066 (10 μM), or THC (40 μM) for 1.5 h before being stimulated by P. a. LPS (0.1 μg/ml) for 24 h. ELISA was used to detect the production of (a) IL-6, (b) TNF-α, (c) MIP-2, (d) IP-10, and (e) nitrite from BV2 microglial cells under P. a. LPS stimulation. The experimental quantitative data are presented in terms of the mean ± SD (n = 3). Bars with the same letter represent no significant difference between the groups. Bars with different letters indicate a statistically significant (p < 0.05) difference between the groups.
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