Effect of endoplasmic reticulum protein 29 on cerebral injury secondary to intracerebral hemorrhage in rats
- Author:
- No author available
- Journal Title:
- Chinese Journal of Neuromedicine
- Issue:
- 9
- DOI:
- 10.3760/cma.j.issn.1671-8925.2011.09.002
- Key Word:
- 脑出血;内质网蛋白29;Bip/GRp78;内质网应激反应;Cerebral hemorrhage;Endoplasmic reticulum protein 29;Bip/GRp78;Endoplasmie reticulum stress response
Abstract： Objective To investigate the expression changes of endoplasmic reticulum protein 29 (ERp29) in the rat brain tissue after cerebral hemorrhage, and explore its role in cerebral injury secondary to intracerebral hemorrhage.Methods Sixty SD rats, weighting (200±20) g, were randomly divided into normal control group (n=10) and cerebral hemorrhage group (n=50); rat models in the cerebral hemorrhage group were induced by stereotactic injection of autologous blood into the caudate nucleus. RT-PCR and Western blotting were employed to detect the mRNA and protein expressions of ERp29 and endoplasmic reticulum chaperones BIp/GRp78 at 6, 12, 18, 24 and 48 h after the inducement. Results The mRNA and protein expressions of BIp/GRp78 began to increase 12 h after the inducement, and gradually increased with the time prolongation, reaching their peak levels at 48h after the inducement, which were significantly different as compared with those in the normal control group (P≤0.05). The mRNA and protein expressions of ERp29 in the cerebral hemorrhage group at 6 and 12 h after the inducement showed no obvious changes as compared with those in the control group (P＞0.05), while the mRNA and protein expressions of ERp29 in the cerebral hemorrhage group 18, 24 and 48 h after the inducement were obviously increased as compared with those in the control group (P≤0.05).Conclusion The endoplasmic reticulum stress response is activated in the surrounding brain tissue of hematoma and the expressions of ERp-29 is up-regulated at this process, which indicates that ERp-29might play a protective role and interact with Bip/GRp78 to inhibit the process of endoplasmic reticulum stress response so as to decrease the damaged effect of hematoma to the surrounding brain tissue.
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