Propofol Protects Hippocampal Neurons from Hypoxia-Reoxygenation Injury by Decreasing Calcineurin-Induced Calcium Overload and Activating YAP Signaling

Figure 2

Propofol reversed H/R-induced intracellular calcium accumulation and MMP loss by inhibiting calcineurin activity and FKBP12.6-RyR disassociation. HT-22 cells were pretreated without or with different concentrations of propofol for 2 hr prior to stimulation by H/R. (a) Intracellular calcium was assessed by the calcium indicator, Fura-2/AM. Typical images of Fura-2A/M staining were captured. Columns indicate the measured mean fluorescent intensities of Fura-2A/M staining in HT-22 cells. (b) MMP measurements were detected by flow cytometry. Columns indicated the measured mean fluorescent intensities of rhodamine 123 staining in HT-22 cells. (c) Columns demonstrated the detected enzymatic activity of calcineurin in HT-22 cells. (d) FKBP12.6-RyR disassociation in HT-22 cells was detected by coimmunoprecipitation. RyR3 was immunoprecipitated with FKBP12.6 antibody and immunoblotted with FKBP12.6 antibody. Columns indicate the molecular recruitment of FKBP12.6. (^aDifferences were significant when compared with “control,” . ^bDifferences were significant when compared with “H/R,” . ^cDifferences were significant when compared with “H/R + 5 μmol/l,” . ^dDifferences were significant when compared with “H/R + 10 μmol/l,” .)

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