The protective mechanism of Naoxintong on cerebral ischemic injury in rats
- Author:
Hong-Ju ZHANG
1
Author Information
1. Department of Neurology
- Publication Type:Journal Article
- From:
Academic Journal of Second Military Medical University
2006;27(2):165-168
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To observe the influence of Naoxintong on expression of glucose-regulated protein 78(GRP78) and GRP94 in the striatum of rats with focal cerebral ischemic injury, so as to investigate their possible protective mechanism on cerebral ischemic injury. Methods: Ninety rats were equally randomized into 3 groups(n=30): sham operated group, ischemic group (Focal transient cerebral ischemia model was established with intraluminal occlusion of left middle cerebral artery) and Naoxintong pre-treated group (Treated with Naoxintong 5 d before ischemic injury). The expression of GRP78, GRP94 in rats striatum was detected by histological method, immunohistochemistry staining and semiquantitative RT-PCR at the different time points(6,12 and 24 h after ischemic treatment). Results: The focal transient cerebral ischemia model was successfully established in rats. Histological results showed that the degree of focal cerebral ischemic injury in Naoxintong pre-treated group was significantly lower than that in ischemic group. Immunohistochemistry staining and RT-PCR results illustrated that the expression of GRP78 and GRP94 in ischemic group was lower than that in sham operated group at each time point after ischemic treatment (P<0.01). The expression of GRP78 and GRP94 in ischemic group and Naoxintong pre-treated group were the lowest at 6 h and the highest at 12 h, and the expression at 24 h was lower than that at 12 h but higher than that at 6 h. Compared with the ischemic group, the expression of GRP78 and GRP94 was higher in Naoxintong pre-treated group at the same time point (P<0.05,P<0.01). Conclusion: The expression of GRP78 and GRP94 is upregulated within 12 h of cerebral ischemic injury in rats. Naoxintong can promote the expression of GRP78 and GRP94 in ischemic cerebral areas, protect the function of endoplasmic reticulum and relieve the cerebral injury caused by ischemia.
