Fig 1: THC reduces the production of IL-6, TNF-a, MIP-2, IP-10, and nitrite in P. a. LPS–stimulated BV2 microglial cells. BV2 microglial cells were untreated (the mock group) or pretreated with THC (10, 20, or 40 µM) for 1.5 h before being stimulated by P. a. LPS (0.1 µg/ml) for 24 h. The production of (a) IL-6, (b) TNF-a, (c) MIP-2, (d) IP-10, and (e) nitrite was detected using ELISA. The experimental quantitative data are presented in terms of the mean ± SD (n = 3). The mock group was considered as a control group. 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 2: STAT3/JAK blocker combined with THC reduces IL-6, TNF-a, 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-a, (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.
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-NF?B expression. THC also inhibits the level of P. a. LPS–prompted JAK-STAT signaling and the inflammatory mediators IL-6, TNF-a, MIP-2, and IP-10 productions. Collectively, THC is a potent anti-inflammatory agent in brain encephalitis.
Supplier Page from Abcam for Mouse MIP2 Matched Antibody Pair Kit