Interferon-γ priming enhances the therapeutic effects of menstrual blood-derived stromal cells in a mouse liver ischemia-reperfusion model

Figure 8 Indoleamine 2,3-dioxygenase secreted by interferon-γ-primed menstrual blood-derived stromal cells enhanced autophagy by inhibiting the mammalian target of rapamycin pathway and activating the AMPK pathway. A: Immunofluorescence images of GFP-LC3. Scale bar 2 μm; B: The number of intense punctate GFP-LC3 aggregates in each cell was counted to determine the level of autophagy in each group. The data are expressed as the means ± SEMs (n = 10/group); C: The expression of p-AMPK, AMPK, p-mammalian target of rapamycin (p-mTOR), mTOR, LC3, and ACTB in L02 cells was determined by western blotting; D: The relative normalized protein expression was quantified based on the intensities of the western blot bands (n = 3/group). The data are presented as the means ± SEMs. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001, ^dP < 0.0001. NS represents not statistically significant. All P values were obtained by one-way ANOVA. NC: Negative control; 3MA: 3-methyladenine; 1MT: 1-methyl-D-tryptophan; MenSCs: Menstrual blood-derived stromal cells; IFN-γ: Interferon-γ; HR: Hypoxia/reoxygenation; HRM: Combination treated with hypoxia/reoxygenation and menstrual blood-derived stromal cells; HRM (IFN-γ): Combination treated with hypoxia/reoxygenation and I interferon-γ-primed menstrual blood-derived stromal cells; AMPK: AMP-activated protein kinase; mTOR: the Mammalian target of rapamycin signaling pathway.