Abstract
Aims & Objectives: This study aimed to investigate the role of CGRP in LPS-induced ALI in ratsthis study aimed to investigate the role of CGRP in LPS-induced ALI in rats. Methods In the experiment, Sprague-Dawley (SD) rats were randomized into control, CGRP8-37, LPS groups and CGRP8-37+LPS groups. ALI model was prepared through retrograde injection of LPS (10mg/kg). At 6h and 12h, bronchoalveolar lavage was performed and used to assess total cell count and levels of tumor necrosis factor- α, interleukin-1β, -6, and -10 by enzyme-linked immuosorbent assay (ELISA). Lung tissue was collected for assessing wet-to-dry (W/D) ratio, hematoxylin and eosin staining. AQP-1 and -5 expressions in lung tissues were detected by quantitative PCR and Western blot. Results The results showed that histological injury, total cell count and W/D ratio significantly reduced. The levels of inflammatory cytokine in CGRP8-37+LPS treated rats were higher than that in LPS rats (all, p<0.001). Real-time RT-PCR analysis showed that AQP-1 and -5 expression in CGRP8-37+LPS rats was lower than that in LPS rats (p=0.005 and p<0.001). Conclusions Our data suggest that CGRP antagonists, CGRP8-37 could enhance ALI induced by LPS in a rat model, and regulate the expression levels of AQP-1 and AQP-5 by affecting inflammatory cytokine. Thereby regulating endogenous CGRP maybe a potential treatment for ALI/ARDS.
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