Astragaloside IV regulates TL1A and NF-KB signal pathway to affect inflammation in necrotizing enterocolitis

Aim: This study aims to explore the possible effect of Astragaloside IV (AS-IV) on necrotizing enterocolitis (NEC) neonatal rat models and verify the possible implication of TNF-like ligand 1 A (TL1A) and NF-KB signal pathway.Methods: NEC neonatal rat models were established through formula feeding, cold/asphyxia stress and Lipo-polysaccharide (LPS) gavage method. The appearance, activity and skin as well as the pathological status of rats subjected to NEC modeling were assessed. The intestinal tissues were observed after H & E staining. The expression of oxidative stress biomarkers (SOD, MDA and GSH-Px) and inflammatory cytokines (TNF-& alpha;, IL-113 and IL-6) were detected by ELISA and qRT-PCR. Western blotting and immunohistochemistry were applied to detect expressions of TL1A and NF-KB signal pathway-related proteins. Cell apoptosis was assessed by TUNEL. Results: NEC neonatal rat models were established successfully, in which TL1A was highly expressed and NF-KB signal pathway was activated, while TL1A and NF-KB signal pathway can be suppressed by AS-IV treatment in NEC rats. Meanwhile, inflammatory response in intestinal tissues was increased in NEC rat models and AS-IV can attenuate inflammatory response in NEC rats through inhibiting TL1A and NF-Kb signal pathway.Conclusion: AS-IV can inhibit TL1A expression and NF-Kb signal pathway to attenuate the inflammatory response in NEC neonatal rat models.

Automated summary

The aim of this study was to investigate the potential impact of Astragaloside IV (AS-IV) on neonatal rat models with necrotizing enterocolitis (NEC) and to confirm the potential involvement of TNF-like ligand 1 A (TL1A) and the NF-KB signaling pathway. NEC neonatal rat models were induced through formula feeding, cold/asphyxia stress, and Lipo-polysaccharide (LPS) administration. The appearance, behavior, skin condition, and pathological status were evaluated in the NEC-modelled rats. Intestinal tissues were examined using H&E staining. The expression of oxidative stress biomarkers (SOD, MDA, GSH-Px) and inflammatory cytokines (TNF-α, IL-13, IL-6) were measured using ELISA and qRT-PCR. TL1A and NF-KB signaling pathway-related proteins were detected using Western blotting and immunohistochemistry. Cell apoptosis was assessed using TUNEL. The results showed that successful NEC neonatal rat models were established, with high expression of TL1A and activation of the NF-KB signaling pathway. AS-IV treatment suppressed TL1A and the NF-KB signaling pathway in NEC rats. Moreover, AS-IV attenuated the inflammatory response in the intestinal tissues of NEC rats by inhibiting TL1A and the NF-Kb signaling pathway.