Skip to main content
Fig. 9 | Journal of Neuroinflammation

Fig. 9

From: α1-antitrypsin mitigates NLRP3-inflammasome activation in amyloid β1–42-stimulated murine astrocytes

Fig. 9

Treatment with A1AT time-dependently mitigated Aβ1–42-induced upregulation of IL1β-precursor protein in primary astrocytes. Western blot confirmed an Aβ1–42-induced significant increase of of IL1β-precursor protein at 3 h (a) and 6 h (b). Co-treatment with A1AT significantly attenuated this increase at 3 h and 6 h stimulation time. Addition of MCC950 did not alter levels of IL1β-precursor protein in Aβ1–42-stimulated astrocytes. A1AT + in Aβ1–42 in the presence of MCC950 did not alter IL1β-precursor protein levels at both 3 h and 6 h. (cd) IL-1β-ELISA revealed a time-dependent upregulation of IL-1β protein levels in Aβ1–42-stimulated astrocytes, significant at 6 h stimulation. Co-treatment with A1AT significantly decreased protein expression of IL-1β time-dependently, at 6 h stimulation time. The presence of MCC950 in Aβ1–42-stimulated decreased IL-1β-expression significantly at both 3 h and 6 h. Further, there is a trend towards a decrease of IL-1β-protein levels in the presence of MCC950 in nearly all treatment groups, though not significant. Co-stimulation of Aβ1–42 and A1AT in MCC950-pretreated astrocytes did not affect IL-1β-expression. Data of n = 3 in triplicate represent mean ± SD. */ap < 0.05; **/aap < 0.01; ***/aaap < 0.001, ns not significant compared to untreated cell control (ctr)

Back to article page