Fig. 3
From: α1-antitrypsin mitigates NLRP3-inflammasome activation in amyloid β1–42-stimulated murine astrocytes
Treatment with A1AT abrogated Aβ1–42-induced upregulation of NLRP3 mRNA and protein in primary astrocytes. a As quantified by RT-PCR treatment with 4 μM and 10 μM of Aβ1–42 significantly increased mRNA levels of NLRP3 in astrocytes. In addition, co-treatment with 4 mg/mL of A1AT blocked this increase in NLRP3 mRNA expression significantly. Data of n = 6 in triplicate represent mean ± SD. b–c Densitometric analysis of western blots confirmed an Aβ1–42-induced significant increase of NLRP3 protein levels at 3 h. Treatment with 4 mg/mL of A1AT significantly attenuated this increase at 10 μM Aβ1–42. Data of n = 3 in triplicate represent mean ± SD. d–e Astrocytes treated with 10 μM of Aβ1–42 showed a significant increase of NLRP3-fluorescence intensity, whereas co-treatment with A1AT significantly reduced NLRP3-expression. Fluorescence images of each experiment were taken using the exact same microscope settings and fluorescence intensity was measured by ImageJ (USA). Data of n = 4 in triplicate represent mean ± SD. */ap < 0.05; **/aap < 0.01; ***/aaap < 0.001, ns not significant compared to untreated cell control (ctr)