2019
Subarachnoid hemorrhage induced cellular and enzymatic changes in the choroid plexus
SOLÁR, Peter, Petr DUBOVÝ, Radim JANČÁLEK a Marek JOUKALZákladní údaje
Originální název
Subarachnoid hemorrhage induced cellular and enzymatic changes in the choroid plexus
Autoři
SOLÁR, Peter (703 Slovensko, domácí), Petr DUBOVÝ (203 Česká republika, domácí), Radim JANČÁLEK (203 Česká republika, domácí) a Marek JOUKAL (203 Česká republika, garant, domácí)
Vydání
Morphology 2019, 2019
Další údaje
Jazyk
angličtina
Typ výsledku
Konferenční abstrakt
Obor
30106 Anatomy and morphology
Stát vydavatele
Slovensko
Utajení
není předmětem státního či obchodního tajemství
Kód RIV
RIV/00216224:14110/19:00112335
Organizační jednotka
Lékařská fakulta
ISBN
978-80-8152-758-6
Klíčová slova anglicky
Subarachnoid hemorrhage; choroid plexus
Štítky
Změněno: 29. 1. 2020 11:25, Mgr. Tereza Miškechová
Anotace
V originále
Introduction: The subarachnoid hemorrhage (SAH) is a specific form of hemorrhagic stroke. Choroid plexus (CP) of the brain ventricles forms the blood – cerebrospinal fluid barrier and is responsible for producing cerebrospinal fluid. The aim of our study was to describe the cellular and enzymatic changes after SAH or application of artificial cerebrospinal fluid (ACSF). Material and methods: SAH was induced by application non-heparinized autologous blood (SAH group) or ACSF (ACSF group) into the cisterna magna and animals were left to survive for 1, 3 and 7 days. The brain sections of naive, SAH and ACSF groups of animals were immunostained under identical conditions with anti-CD68 (ED1), anti-CD163 (ED2), anti-CCR7, anti-CD206, anti-CD3, anti MHC II, anti-Ki67, anti- heme-oxygenase-1 (HO-1), and anti-biliverdin reductase (BVR) antibodies. Immunohistochemical staining of HO-1 and BVR was confirmed by Western blot analysis. Results: The number of MHC II+ cells as well as ED1+ macrophages increased with duration after SAH or ACSF application while the number of ED2+ macrophages showed increased in all periods following SAH. Immunostaining of CCR7+ cells showed gradually decreased in both groups of animals. The number of CD206+ cells showed increased with duration after SAH and decreased after ACSF injection. CD3 immunostaining did not reveal T cells in the CP of any group of the animals. Ki-67 immunostaining showed gradually increased proliferation following SAH and decreased with duration after ACSF application. Increased expression of HO-1 and BVR was found in all periods following SAH. Conclusions: Our results demonstrate that CP responds with immune cellular and enzymatic changes at different time periods following the application of blood or ACSF. These findings indicate that not only blood degradation products but also increased intracranial pressure after SAH contributes to cellular and enzymatic changes in the CP following SAH.
Návaznosti
MUNI/A/1086/2018, interní kód MU |
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