Figure 3.
Efavirenz treatment alters cellular function in LX2 cells, thus promoting their activation. (A) Quantitative analysis of mitochondrial function by fluorescence microscopy: mitochondrial membrane potential (TMRM fluorescence), mitochondrial superoxide production (MitoSOX fluorescence), mitochondrial morphology and mass (NAO fluorescence) (n = 5). (B) Assessment of unfolded protein response and endoplasmic reticulum stress: quantitative analysis of the endoplasmic reticulum signal (ER-Tracker Red fluorescence) and protein expression of the classic markers of these processes, GRP78 and CHOP. Representative Western Blot image of these proteins and summary of densitometry data after 24 h treatment (n = 5–6). (C) Assessment of cellular proliferation/viability: quantitative analysis of cell number (Hoechst 33342-nuclei) and nuclear fluorescence intensity (n = 6). Data were represented as mean ± SEM, calculated as percentage of control (untreated cells) and analyzed by one-way ANOVA multiple comparison test followed by a Newman–Keuls test (* p < 0.05, ** p < 0.01, *** p < 0.001 versus the respective vehicle). Thapsigargin (TG), rotenone (Rot) and cocktail of LPS (C.LPS) were independently analyzed by a Student’s t-test (# p < 0.05, ## p < 0.01, ### p < 0.001).