Fig. 7.

Pharmacological inhibition of AMPKα with compound C or expression of dominant negative AMPKα attenuates upregulation of NOX2 and its regulatory proteins, generation of H₂O₂, as well as apoptosis in PD toxins-induced neuronal cells. PC12 cells and primary neurons, or PC12 cells infected with Ad-dn-AMPKα or Ad-LacZ (as control), respectively, were treated with/without 6-OHDA (120 μM), MPP⁺ (1 mM) or rotenone (1 μM) for 24 h following pre-incubation with/without compound C (20 μM) for 2 h, or treated with/without 6-OHDA (120 μM), MPP⁺ (1 mM) or rotenone (1 μM) for 24 h. A and D Total cell lysates were subjected to western blotting using indicated antibodies. The blots were probed for β-tubulin as a loading control. Similar results were observed in at least three independent experiments. B and E Intracellular H₂O₂ was imaged and quantified using a peroxide-selective probe H₂DCFDA. C and F Apoptotic cells were evaluated by nuclear fragmentation and condensation using DAPI staining. Results were presented as mean ± SEM, n = 5. ^aP < 0.05, difference with control group; ^bP < 0.05, + Compound C group vs - Compound C group; ^cP < 0.05, Ad-dn-AMPKα group vs Ad-LacZ group.