Related Experiment Video
Updated: Dec 30, 2025
A Model of Acute Lung Injury Following Visceral Ischemia-Reperfusion by Supra-Coeliac Aortic Cross Clamping in Rats
Published on: August 15, 2025
Transient cerebral ischemia/reperfusion-induced acute lung injury in rats associated with protein kinase C alpha
Sai-Bin Wang1, Qian Ye2, Jun-Wei Tu1
1Department of Respiratory Medicine, Jinhua Municipal Central Hospital, Jinhua Hospital of Zhejiang University Jinhua, Zhejiang Province, P. R. China.
Objective:
The pathogenesis and development timing of acute lung injury (ALI) following cerebral ischemia/reperfusion (I/R) are not fully understood. In this study, the development timing of ALI induced by transient global cerebral I/R as well as the underlying mechanisms of action were investigated.
Methods:
A cerebral I/R-induced ALI model in Wistar rats was established by electrocoagulation of bilateral vertebral arteries combined with ligation of the transient bilateral common carotid arteries. Rats were randomly divided into control and cerebral I/R groups. The latter was subdivided into 3 h, 24 h, 48 h and 72 h post reperfusion. Lung injury was assessed by histological examination. The mRNA and protein expression of protein kinase C alpha (PKCα) were determined using qRT-PCR and immunofluorescence analysis, respectively.
Results:
Lung histological injury could be detected as early as 3 h after global cerebral I/R, and was significant between groups at 48 h and 72 h. Compared with the control group, mRNA expression of PKCα in the lung was enhanced in rats in the cerebral I/R groups (P<0.001), and the highest expression was observed at 48 h (P<0.001). The intensity of PKCα reactivity gradually increased starting at 3 h, and peaked at 72 h after cerebral I/R (P<0.05).
Conclusions:
The lung is very susceptible to transient global cerebral I/R injury in vivo. Lung histological injury occurred within hours of cerebral I/R induction and aggregated in a very short period after cerebral I/R. Moreover, PKCα expression was implicated in the pathogenesis of cerebral I/R-induced ALI.
