2017
Inflammatory changes in the choroid plexus after paclitaxel treatment
SINAI CACODCAR, Rahul Sanjiva, Adriana SLANÍKOVÁ, Michael LUJC, Ilona KLUSÁKOVÁ, Petr DUBOVÝ et. al.Základní údaje
Originální název
Inflammatory changes in the choroid plexus after paclitaxel treatment
Název česky
Zánětlivé změny choroidního plexu po léčbě paklitaxelem
Autoři
SINAI CACODCAR, Rahul Sanjiva, Adriana SLANÍKOVÁ, Michael LUJC, Ilona KLUSÁKOVÁ, Petr DUBOVÝ a Marek JOUKAL
Vydání
Morphology 2017, 2017
Další údaje
Jazyk
angličtina
Typ výsledku
Prezentace na konferencích
Obor
30000 3. Medical and Health Sciences
Stát vydavatele
Česká republika
Utajení
není předmětem státního či obchodního tajemství
Organizační jednotka
Lékařská fakulta
ISBN
978-80-263-1315-1
Klíčová slova česky
Paclitaxel, krevně-likvorová bariéra, plexus choroideus, neuropatie, makrofágy, TLR9 , ED1, ED2
Klíčová slova anglicky
Paclitaxel, blood-cerebrospinal barrier, plexus choroideus, neuropathy, macrophages, TLR9, ED1, ED2
Změněno: 5. 10. 2017 15:47, MUDr. Rahul Sanjiva Sinai Cacodcar
Anotace
V originále
Peripheral neuropathy as a side effect of chemotherapeutic agent Paclitaxel is caused by disorders of calcium homeostasis and mitochondrial damage in axons. These changes are associated with release of damage associated molecular patterns to the blood stream with potential effect on the blood-cerebrospinal fluid (B-CSF) barrier presented in choroid plexus (CP) of the brain ventricles. The aim of our work was to study the cellular and the molecular changes in the CP after intraperitoneal administration of Paclitaxel. Wistar rats (n=23, males) were used in our experiments. Intraperitoneal injection of Paclitaxel in 4 doses with cumulative dose 8 mg/kg was performed in experimental rats while control animals received vehiculum (alcohol and cremophor; 1:1). The animals were left to survive for 1, 3, 7 and 14 days from the last application. Experimental and control rats were sacrificed together with naïve rats and perfused transcardially by Zamboni´s fixative. Cryostat coronal sections through the brain were cut and immunostained for activated (ED1) and resident (ED2) macrophages as well as for Toll-like Receptors 9 (TLR-9). Numbers of ED1+ and ED2+ cells per 1 mm2 and intensity of TLR9 immunofluorescence in CP were counted and statistically analyzed. Presence of ED1+ and ED2+ macrophages was observed in epiplexus position of CP. Statistically significant increased numbers of ED1+ and ED2+ macrophages comparing to naïve and control rats were found in the CP after administration of Paclitaxel. Number of ED1+ cells increased with time of survival. TLR-9 immunofluorescence was presented in cytoplasm of the cuboidal cells and its immunofluorescence intensity increased with time after the last application. Our results clearly indicate that intraperitoneal administration of Paclitaxel induces inflammatory response in CP expressed by increased numbers of macrophages and expression of TLR-9 following the time from the last application.
Návaznosti
MUNI/A/0973/2016, interní kód MU |
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