Anti-Tn Monoclonal Antibody Ameliorates Hyperoxia-Induced Kidney Injury by Suppressing Oxidative Stress and Inflammation in Neonatal Mice

Figure 3

(a, c) Representative immunohistochemistry and (b, d) Western blot analysis of NF-κB and IκB-α in the RA-reared and hyperoxia-reared rats treated with PBS or anti-Tn monoclonal antibodies on postnatal day 7. The immunoreactivity of NF-κB-p65 (black arrow) and IκB-α (black arrow) was primarily detected in the podocytes of the glomerulus and the tubular cells of kidney tissue. The mice reared in hyperoxia and treated with PBS exhibited a higher number of positive NF-κB-p65 and fewer positive IκB-α cells. Anti-Tn monoclonal antibody treatment significantly reduced the hyperoxia-induced increase in NF-κB expression and increased the hyperoxia-induced decrease in IκB-α expression. , .

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