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. Author manuscript; available in PMC: 2014 Jun 25.
Published in final edited form as: J Alzheimers Dis. 2014 Jan 1;41(2):499–513. doi: 10.3233/JAD-132792

Fig. 9.

Fig. 9

Propofol attenuates Aβ-induced mPTP opening through GABA receptor in N2A cells. A) Flow cytometric analysis shows changes in calcein levels in mitochondria of N2A cells stained with calcein AM or calcein AM plus cobalt, which indicate the opening of the mPTP. Peak 1: positive control cells (treatment of calcein AM plus cobalt and ionomycin); peak 2: negative control (treatment of calcein AM plus cobalt); peak 3: cells treated with calcein AM plus cobalt and 5 μM Aβ; peak 4: cells treated with calcein AM plus cobalt and 5 μM Aβ and 100 μM propofol. The changes in intensity of fluorescence between Aβ treated (peak 3), Aβ plus propofol (peak 4), positive control (peak 1), and negative control (peak 2) suggest that Aβ induces the opening of the mPTP, propofol attenuates the Aβ-induced opening of the mPTP, as demonstrated by that the position of peak of Aβ treatment is shifted to right following the propofol treatment. B) Peak 1: positive control (treatment of calcein AM plus cobalt and ionomycin); peak 2: negative control (treatment of calcein AM plus cobalt); peak 3: cells treated with calcein AM plus cobalt and 5 μM Aβ and 100 μM propofol; peak 4: cells treated with calcein AM plus cobalt and 5 μM Aβ plus 100 μM propofol and 20 μM flumazenil. The changes in intensity of fluorescence between Aβ plus propofol (peak 3), Aβ plus propofol and flumazenil (peak 4), positive control (peak 1), and negative control (peak 2) suggest that flumazenil inhibits the attenuation effect of propofol on the Aβ-induced opening of the mPTP in N2A cells. mPTP, mitochondrial permeability transition pore, Aβ, amyloid-β protein. n = 6.