Early changes in GMRP1 after intracerebral hemorrhage: involvement in brain damage and cell apoptosis.

Glucose metabolism-related protein 1 (GMRP1), also known as BTBD10, has been reported to inhibit apoptosis of neuronal and islet beta cells via the Akt pathway. The present study attempted to investigate whether GMRP1 and its mediated Akt pathway were involved in brain injury of rats after intracerebral hemorrhage (ICH). Rat models of ICH had been established successfully. Western blotting was used to investigate the levels of GMRP1 protein in the caudate nuclei tissues of the hemorrhagic and contralateral sides at 6 h, day 1, day 3, day 5, and day 7 after ICH. Phosphorylations of Akt was determined in caudate nuclei mentioned above. TUNEL assay was used to measure the cell apoptosis. GMRP1 protein levels, as well as phosphorylations of Akt, significantly decreased in caudate nuclei of the hemorrhagic side, compared with those of the contralateral side on day 1 and day 3 after ICH. Enhanced cell apoptosis was observed on the hemorrhagic side using TUNEL assay. We presented here evidence that a decreased GMRP1-mediated Akt pathway contributed to cell apoptosis on the hemorrhagic side, suggesting that GMRP1 plays an important role in brain damage after ICH.