Dexmedetomidine protects rats from postoperative cognitive dysfunction via regulating the GABA R-mediated cAMP-PKA-CREB signaling pathway.

This work attempts to discuss whether dexmedetomidine (Dex) can protect rats from postoperative cognitive dysfunction (POCD) through regulating the γ-aminobutyric acid- receptor (GABA R)-mediated cyclic adenosine monophosphate (cAMP) - protein kinase A (PKA) - cAMP-response element binding (cAMP-PKA-CREB) signaling pathway. Sprague-Dawley rats were divided into a non-surgical group (Control), a surgical group (Model), a surgical group treated with Dex (Model + Dex), a surgical group treated with GABA R antagonist (Model + CGP 35348) and a surgical group treated with Dex and GABA R agonist (Model + Dex + Baclofen). Cognitive and memory functions were evaluated by Y-maze test and open-field test.

Regulation on the expression of Clara cell secretory protein in the lungs of the rats with acute lung injury by growth hormone.

Background: Clara cell secretory protein (CC16) is an important lung derived protective factor and may play an important role on the pathogenesis of acute lung injury (ALI) induced by endotoxemia. Growth hormone (GH) is an important anabolism hormone secreted by GH cells of the hypophysis. Previous research showed that GH would significantly exacerbate ALI induced by endotoxemia, but the mechanism is not very clear yet.

[The effect of growth hormone on Clara cell in acute lung injury of rats].

Objective: To study the effect of growth hormone (Gh) on Clara cell in acute lung injury (ALI) rats during stress responsive stage.

Methods: One hundred and twelve male Sprague-Dawley (SD) rats were randomly divided into ALI group and recombinant human Gh (rhGh) group. The rats in two groups were subdivided into seven subgroups of different time intervals after lipopolysaccharide (LPS) injection:0 (pre-injection of LPS, acted as control group), 0.

[Effect of growth hormone on acute lung injury].

Objective: To study the effect of growth hormone (GH) on acute lung injury (ALI) induced by endotoxemia, and its potential therapeutic mechanism.

Methods: One hundred and twelve male Sprague-Dawley rats were randomly divided into ALI group and GH group. The rats in two groups were further divided into seven subgroups determined by the length of interval after lipopolysaccharide (LPS) challenge: 0 (before injection of LPS, served as control group), 0.