Figure 2
Figure 2. Sirt1 regulates NF-κB acetylation/activation and lung inflammation after PM2.5 exposure. Sirt1+/+ and Sirt1−/− littermates were exposed to PBS or PM2.5 (100 μg) by intranasal instillation. (A) Six hours later, lung homogenates prepared were subjected to immunoblotting to examine NF-κB acetylation (Ace-NF-κB). Blots are representative of 5 mice in each experimental group. (B) NF-κB DNA binding activity was measured by ELISA. Data are presented as mean + SEM (n ≥ 7 mice/group; *P < .05). (C) Sirt1+/+ and Sirt1−/− littermates were exposed to PBS or PM2.5 (100 μg) by intranasal instillation. Twenty-four hours later, BAL TNF-α and IL-6 levels were assessed by ELISA. Data are presented as mean + SEM (n = 7 mice/group; *P < .05).

Sirt1 regulates NF-κB acetylation/activation and lung inflammation after PM2.5 exposure. Sirt1+/+ and Sirt1−/− littermates were exposed to PBS or PM2.5 (100 μg) by intranasal instillation. (A) Six hours later, lung homogenates prepared were subjected to immunoblotting to examine NF-κB acetylation (Ace-NF-κB). Blots are representative of 5 mice in each experimental group. (B) NF-κB DNA binding activity was measured by ELISA. Data are presented as mean + SEM (n ≥ 7 mice/group; *P < .05). (C) Sirt1+/+ and Sirt1−/− littermates were exposed to PBS or PM2.5 (100 μg) by intranasal instillation. Twenty-four hours later, BAL TNF-α and IL-6 levels were assessed by ELISA. Data are presented as mean + SEM (n = 7 mice/group; *P < .05).

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