Fig. 10

Malva parviflora hydroalcoholic extract regulates the phagocytic capacity of microglial cells via PPARγ-CD36 mediated mechanism. Microglial primary cultures were left untreated or pre-treated with GW9662, a specific PPAR-γ inhibitor for 1 h, following by incubation with MpHE or the PPAR-γ agonist, pioglitazone, at the indicated concentration for 24 h. a The PPAR-γ levels from the cell extracts of microglial primary cultures were determined by immunoblot using specific antibodies and the actin levels were used as internal control. Normalized densitometry values of PPAR-γ (PPAR-γ/actin) present in the extracts of microglial primary cultures in the presence of MpHE (Mp) or pioglitazone and GW9662. Data are shown as mean ± SEM and were analyzed by one-way ANOVA. Ctrl vs Mp 0.1 mg/mL (**p = 0.009); Ctrl vs Mp 1 mg/mL (**p = 0.004); Ctrl vs pioglitazone (**p = 0.001); Mp 0.1 mg/mL vs GW9662 + Mp 0.1 mg/mL (*p = 0.04); Mp 1 mg/mL vs GW9662 + Mp 1 mg/mL (**p = 0.003); Pioglitazone vs GW9662 + Pioglitazone (***p < 0.001). b CD36 mRNA levels were determined by qPCR using total RNA from the microglial primary cultures treated as described above. Data were analyzed by one-way ANOVA. Ctrl vs Mp (*p = 0.04); Ctrl vs pioglitazone (**p = 0.002); Mp vs GW9662 + Mp (*p = 0.04); pioglitazone vs GW9662 + pioglitazone (**p = 0.005). c Representative micrographs from cortex of adult 5XFAD mice alone (Bs) or in the presence of microglial primary cultures (5XFAD Bs + microglia) untreated (−) or pre-treated with M. parviflora or pioglitazone and GW9662. The slices were stained with thioflavin S and analyzed by confocal microscopy. d The plaques number were quantified. Data were analyzed by one-way ANOVA. Bs vs M. parviflora (***p < 0.001); Bs vs pioglitazone (*p = 0.03); M. parviflora vs GW9662 + M. parviflora (*p = 0.04). e The plaques size was quantified. Data were analyzed by one-way ANOVA. Bs vs M. parviflora (*p = 0.03); Ctrl vs M. parviflora (**p = 0.007); M. parviflora vs GW9662 + M. parviflora (*p = 0.02)