Molecular changes in glial cells following subarrachnoidal hemorrhage
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| Year of publication | 2023 |
| Type | Appeared in Conference without Proceedings |
| MU Faculty or unit | |
| Citation | |
| Description | Subarachnoid hemorrhage (SAH) is a subtype of hemorrhagic stroke developing mainly after the rupture of an intracranial aneurysm. In our previous studies, we found cellular and molecular changes in the choroid plexus forming the blood-cerebrospinal barrier after SAH. Following SAH, blood and its degradations products in subarachnoid space also induce a pro-inflammatory reaction in the individual cellular components of the blood-brain barrier and neurovascular unit, mainly in neuroglial cells. The aim of the presented study was to assess the response of microglia in different periods following the induction of SAH or the application of artificial cerebrospinal fluid (ACSF) into the subarachnoid space. Our experiments were performed on Wistar rats (males, 250g). SAH was induced by the injection of autologous arterial blood into the cisterna magna. Increased intracranial pressure induced by SAH was modeled by the application of ACSF into the cisterna magna. The animals in both groups were left to survive 1, 3, 7, and 14 days after application. After a time of survival, the SAH, ACSF, and naive rats were perfused transcardially with Zamboni´s fixative. Coronal cryostat sections through the brains were cut and immunostained for Ox-42 and double immunostained for NFkB. Immunohistochemical staining showed that SAH as well as ACSF application led to increased levels of NFkB in microglia with peaks in 3 days following the application. Morphological examination revealed swollen and more amoeboid forms of microglial cells mainly 3 days following SAH and also ACSF application, but less significantly. Our findings suggest that morphological as well as pro-inflammatory changes in microglial cells occur in the first days following SAH or application of ACSF. These changes are probably caused not only by the blood and blood degradation products but increased intracranial pressure induced by SAH may play an important role. |
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