Idh2 Deficiency Exacerbates Acrolein-Induced Lung Injury through Mitochondrial Redox Environment Deterioration

Figure 6

Protective effects of NAC against acrolein-induced lung damage in idh2^−/− mice. NAC (500 mg/kg) was intraperitoneally administered to idh2^−/− mice 2 h prior acrolein exposure. (a) H&E-stained sections of the lung tissue after acrolein administration. (b) Emphysema in acrolein-treated lung tissues assessed by mean alveolar airspace area (μm²). (c) Lung injury scores were evaluated after acrolein exposure. (d) Immunoblots comparing the levels of apoptotic marker proteins in the lung tissue extracts from idh2^−/− mice. β-Actin was used as an internal control. (e) Immunoblot analysis of Prx-SO₃ levels in the lung tissue extract from idh2^−/− mice. In (b) and (c), data are shown as the mean ± SD ( mice in each group). versus acrolein-treated and NAC-untreated idh2^−/− mice.

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