Fig. 2

Induction of HO-1 protected the lung from LPS-driven mitochondrial oxidative injury. a Cell viability at the indicated conditions was detected by MTT assay. b, d Respiratory control ratio (RCR) levels both in vitro and in vivo. c The survival rate of rats challenged by LPS with or without hemin or LY294002 treatment. Rats (6–10 animals per group) were monitored for lethality for up to 6 h. e Semi-quantification of lung tissues using lung injury scores. A five-point scale was applied to grade the degrees of lung injury based on the pathologic features of alveolar septa edema, airway congestion, interstitium widen or hyaline membrane formation, and neutrophil margination or infiltration: scores of 0 = minimal damage, 1+ = mild damage, 2+ = moderate damage, 3+ = severe damage, and 4+ = maximal damage. Results are expressed as medians (range) using the Mann–Whitney U test. f Photomicrographs of histopathologic changes of lung sections stained with hematoxylin and eosin (original magnification, ×400). Scale bar: 100 μm. g MnSOD activity in lung mitochondria of rats. Data in a and c were analyzed using Mann–Whitney U test followed by Bonferroni correction. Data in b, d, and g were presented as mean ± s.d. using one-way ANOVA corrected with Bonferroni coefficient for multiple comparisons (n = 6 replicates from three independent experiments). Significant differences were indicated with an asterisk: ^*P < 0.05, ^**P < 0.01, ^***P < 0.001. LPS lipopolysaccharide, RCR respiratory control ratio, MnSOD manganese superoxide dismutase, NS not significant