Expression of FPR2 in dorsal root ganglia after Paclitaxel treatment
| Autoři | |
|---|---|
| Rok publikování | 2018 |
| Druh | Konferenční abstrakty |
| Fakulta / Pracoviště MU | |
| Citace | |
| Popis | Paclitaxel, widely used chemotherapeutic agent for solid tumors mainly, causes peripheral neuropathy based on alteration of calcium channels and defragmentation of mitochondria in peripheral nerve axons. N-formylated peptides (fMLP) releasing during mitochondrial damage are associated with the expression of Formyl peptide receptor 2 (FPR2) in dorsal root ganglia (DRG). Our aim was to assess the changes of FPR2 in DRGs related to Paclitaxel application. We used Wistar rats (n=10, males). Intraperitoneal injections of Paclitaxel in 4 doses with a cumulative dose of 8 mg/kg were performed on rats, control animals received vehiculum (alcohol and cremophor; 1:1). The animals were left to survive for 1, 3 and 14 days from the last application. Experimental and control animals were sacrificed together with naive rats and perfused transcardially by Zamboni´s fixative. Longitudinal cryostat sections through the lumbar DRGs were cut and immunostained for FPR2. The intensity of FPR2 immunofluorescence in the DRG was measured and statistically analyzed. FPR2 immunofluorescence was detected in the cytoplasm of neurons and of satellite glial cells surrounding large-sized neurons, in both naive and control animals. Statistically significant increase in FPR2 immunofluorescence was found in the DRGs of Paclitaxel treated animals in comparison to naive animals and in comparison to control animals after the 14 days survival. Also the intensity of FPR2 immunofluorescence increased with the time of survival after the last application. Our results indicate an increase expression of FPR2 in DRGs after Paclitaxel. We suspect these changes are associated with inflammatory reaction in chemotherapy induced peripheral neuropathy. |
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