The role of Cathepsin L in transient forebrain ischemia in rats

Objective To investigate the role of Cathepsin L in transient forebrain ischemia in rats. Methods Seventy healthy male Sprague-Dawley Rats (10~12 weeks old, 260~300 g) were chosen. Based on the random number table method, the rats were randomly divided into sham-operated control group (Sham group, n=10), ischemia-reperfusion group (IRI group, n=25), and Z-FY-DMK intervention group (CLI group, n=25). Rats in groups IRI and CLI were randomly divided into 3 h, 6 h, 12 h, and 24 h subgroups. Modified transient middle cerebral artery occlusion was made as Longa described. The intervention groups were injected intracerebroventricularly Z-FY-DMK (20 μg/μl×5 μl) preoperative 30min prior to surgery. Groups Sham and IRI were injected intracerebroventricularly dimethyl sulfoxide (DMSO) 5 μl (10 ml/L) at the same time. Longa's five level's grading was used to evaluate the neural function defect. 2, 3, 5-Triphenyltetrazolium chloride (TTC) staining method was used to measure infarct volume at 24 h. Western blot was used to detect the expression of Cathepsin L. Results Western blot found there was little visible Cathepsin L protein expression in ischemic cerebral cortex preoptic, Cathepsin L protein expression in IRI group after cerebral ischemia-reperfusion upward at 3 h, 6 h, and 12 h; it reached peak at 12 h, and declined at 24 h, was still higher than the sham group (P<0.01). Cathepsin L protein expression in the CLI group was reduced compared to the IRI group (P<0.05). Conclusions Cathepsin L may be involved in neuronal apoptosis. Key words: Cathepsins/AI/ME; Brain ischemia/ME/PA/DT; Apoptosis/DE