Figure 6.
Figure 6. Pharmacologic activation of A2aR or A3R inhibits LPS-induced TNFα production in vivo. A2aR+/+ (A) and A2aR-/- (B) mice were injected with 0.5 mg/kg of CGS21680, and A3R+/+ (C) and A3R-/- (D) mice were injected intraperitoneally with the 0.5 mg/kg of 2-Cl-IB:MECA. Ten minutes later the mice were injected with 10 mg/kg LPS. The mice were bled 1 hour after LPS injection and the level of TNFα in the serum was measured. This figure shows that LPS-induced TNFα was inhibited by CGS21680 or 2-Cl-IB:MECA in A2aR+/+ (A) and A3R-/- (C) mice, respectively. However, these adenosine receptor-specific agonists did not affect A2aR-/- and A3R-/- mice (B and D, respectively). Representative results from 1 of 3 separate experiments.

Pharmacologic activation of A2aR or A3R inhibits LPS-induced TNFα production in vivo. A2aR+/+ (A) and A2aR-/- (B) mice were injected with 0.5 mg/kg of CGS21680, and A3R+/+ (C) and A3R-/- (D) mice were injected intraperitoneally with the 0.5 mg/kg of 2-Cl-IB:MECA. Ten minutes later the mice were injected with 10 mg/kg LPS. The mice were bled 1 hour after LPS injection and the level of TNFα in the serum was measured. This figure shows that LPS-induced TNFα was inhibited by CGS21680 or 2-Cl-IB:MECA in A2aR+/+ (A) and A3R-/- (C) mice, respectively. However, these adenosine receptor-specific agonists did not affect A2aR-/- and A3R-/- mice (B and D, respectively). Representative results from 1 of 3 separate experiments.

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