Figure 1.
Figure 1. A3 adenosine receptors are required for the inhibition of ConA-induced ALT and TNFα by inosine. C57BL/6 (A-B), A2aR-/- (C-D), A3R-/- (E-F), and A2aA3R-/- (G-H) mice were injected with ConA, inosine (100 mg/kg), or both, and the level of TNFα and ALT in the serum at 1 hour and 24 hours, respectively, after challenge was determined. Because excessive inflammation is observed in the absence of the A2aR,3 A2aR-/- and A2aA3R-/- mice were injected with 15 mg/kg, whereas the C57BL/6 and A3R-/- mice were injected with 20 mg/kg ConA. This figure shows that inosine inhibited ConA-induced hepatitis only in mice expressing the A3R. Representative results from one of 3 separate experiments.

A3 adenosine receptors are required for the inhibition of ConA-induced ALT and TNFα by inosine. C57BL/6 (A-B), A2aR-/- (C-D), A3R-/- (E-F), and A2aA3R-/- (G-H) mice were injected with ConA, inosine (100 mg/kg), or both, and the level of TNFα and ALT in the serum at 1 hour and 24 hours, respectively, after challenge was determined. Because excessive inflammation is observed in the absence of the A2aR, A2aR-/- and A2aA3R-/- mice were injected with 15 mg/kg, whereas the C57BL/6 and A3R-/- mice were injected with 20 mg/kg ConA. This figure shows that inosine inhibited ConA-induced hepatitis only in mice expressing the A3R. Representative results from one of 3 separate experiments.

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