Immunohistochemical evaluations of caspase-3, -8, and -9 revealed significantly reduced apoptosis in the NEC + ABS group compared to the NEC + saline group (p = 0.001).
Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining, cleaved caspase 3, and severity of intestinal injury with NEC were worse in SIGIRR-/- mice in comparison with SIGIRR+/+ mice.ConclusionSIGIRR is a negative regulator of TLR4 signaling in the developing intestine, and its insufficiency results in native intestinal TLR hyper-responsiveness conducive to the development of severe experimental NEC in mice.
Macroscopic evaluation, Histopathologic and apoptosis assessment (TUNEL, caspase 3 and 8) releaved that severity of intestinal damage were significantly lower in the NEC + ginger group (p < 0.05).
It was found that autophagy and apoptosis are both rapidly up regulated in NEC in vivo as indicated by increased expression of the autophagy markers Beclin 1 and LC3II, and by evidence of apoptosis by TUNEL and cleaved caspase-3 staining.