Effect of hirudin on janus kinase 2/signal transducer and activator of transcription 3 signaling pathway in rats with intracerebral hemorrhage L
10.3969/j.issn.1672-5921.2017.12.005
- VernacularTitle:水蛭素对脑出血大鼠蛋白酪氨酸激酶2/信号转导和转录激活因子3信号通路的影响
- Author:
Hong LI
1
;
Lili WU
;
Qing GAO
;
Haihong LI
Author Information
1. 牡丹江医学院临床技能中心
- Keywords:
Hirudin;
Intracerebral hemorrhage;
Apoptosis;
JAK2 / STAT3 signaling pathway;
Rats
- From:
Chinese Journal of Cerebrovascular Diseases
2017;14(12):638-643
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of hirudin on janus kinase 2 / signal transducer and activator of transcription 3 (JAK2 / STAT3)signaling pathway in rats with intracerebral hemorrhage. Methods A total of 216 healthy male Wistar rats were divided into sham operation group,model group, and hirudin group (n =72 in each group)using random digit table. The model of cerebral hemorrhage was induced by injecting autologous arterial blood into the caudate nucleus,and the equal volume isotonic saline was used instead of autologous arterial blood in the sham operation group. Hirudin were injected at 6,24, 72,and 120 h,respectively in the hirudin group,while the sham operation group and the model group were injected with isotonic saline during same period. Neurobehavioral scores,brain water content and brain coefficients of the 3 groups at the different time points were compared. The changes of brain cell apoptosis were detected with annexin V-fluorescein isothiocyanate/ propidium iodide double staining flow cytometry. The expression levels of phosphorylated JAK2 (p-JAK2)and phosphorylated STAT3 (p-STAT3)in brain tissue were detected with Western blot. Results (1)Compared with the sham operation group at same time period,neurobehavioral score,brain water content,brain coefficients,brain cell apoptosis rate,and the expression levels of p-JAK2 and p-STAT3 were increased significantly in the rats of the model group. The differences between the two groups were statistically significant (all P < 0. 05). Compared with the model group at same time period,neurobehavioral score,brain water content,brain coefficients,and brain cell apoptosis rate were decreased significantly in the rats of the hirudin group. The differences between the two groups were statistically significant (all P <0. 05). (2)At 6,24,72,and 120 h after modeling,the expression levels of p-JAK2 were 0. 632 ±0. 036,0. 783 ± 0. 045,1. 250 ± 0. 071,and 1. 006 ± 0. 052,respectively,and those of p-STAT3 were 0. 155 ±0. 005,0. 193 ±0. 006,0. 379 ±0. 012,and 0. 317 ± 0. 010,respectively in model group. The expression levels of p-JAK2 were 0. 267 ± 0. 014,0. 248 ± 0. 013,0. 329 ± 0. 018,and 0. 283 ±0. 016,respectively,and those of p-STAT3 were 0. 139 ± 0. 004,0. 081 ± 0. 001,0. 283 ± 0. 009, and 0. 174 ± 0. 005,respectively in the hirudin group. The expression levels of p-JAK2 and p-STAT3 in hirudin group were lower than those in the model group. There were significant differences between the two groups (all P < 0. 05). Conclusion Hirudin can reduce apoptosis of brain cells after intracerebral hemorrhage in rats,its protective mechanism may be associated with the inhibition of JAK2 / STAT3 signaling pathway.
