Expression of NGF, proNGF, p75NTR in lung injury induced by cerebral ischemia-reperfusion in young and elderly rats

Abstract

Objective: This study aims to investigate the expression levels of Nerve Growth Factor (NGF), the precursor form of NGF (proNGF), and p75 neurotrophin receptor (p75NTR) in lung injury induced by cerebral IschemiaReperfusion (I/R) in both young and elderly rats. Methods: Male Sprague-Dawley rats, categorized as young (3-months-old) and elderly (16-months-old), were divided into four experimental groups: Young Sham, Young I/R, Elderly Sham, and Elderly I/R. Each group underwent either sham surgery or ischemia-reperfusion treatment. Following 24 h post-procedure, the severity of cerebral ischemia was assessed using the Zea Longa 5-point scoring system, and lung tissue pathological changes were examined using Hematoxylin and Eosin (HE) staining. Western blot analysis was utilized to measure the expression levels of NGF, proNGF, and p75NTR proteins in lung tissue. Results: Both young and elderly I/R groups exhibited lung tissue congestion and edema compared to their respective sham groups, with a significant increase in pathological scores (p < 0.05). Furthermore, the elderly I/R group demonstrated a significantly higher pathological score compared to the young I/R group (p < 0.05). Western blot analysis revealed that compared to the young sham group, the expression of NGF in the lung tissue of elderly sham rats decreased (p < 0.05), while proNGF and p75NTR increased (p < 0.05). Additionally, compared to the sham group, the levels of NGF, proNGF, and p75NTR in lung tissue were elevated in both young and elderly I/R groups of rats (p < 0.05). Moreover, the expression of proNGF and p75NTR in lung tissue was higher in the elderly I/R group than in the young I/R group (p < 0.05). Conclusion: Cerebral ischemia-reperfusion-induced lung injury was associated with increased expression of proNGF and p75NTR, as well as decreased NGF expression in lung tissue. These alterations in NGF, proNGF, and p75NTR may contribute to the susceptibility to age-related lung injury.