Publication details
Inflammatory reactions in the dorsal root ganglia of rats with paclitaxel-induced neuropathy
| Authors | |
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| Year of publication | 2013 |
| Type | Conference abstract |
| MU Faculty or unit | |
| Citation | |
| Description | Paclitaxel, chemotherapeutic agents used for the treatment of solid tumors, results in many patients in peripheral neuropathy often accompanied with neuropathic pain. Mechanisms responsible for the development of neuropathic pain are still not well understood. The aim of present study was investigate the cellular and molecular changes in dorsal root ganglion (DRG) of rat model of paclitaxel-induced neuropathic pain. Six rats were treated with cumulative dosage of Paclitaxel 2mg/kg and survived for 3 and 7 days from last administration. Three naive rats served as control. The cryostat sections through cervical and lumbar DRG was incubated under the same conditions with antibodies against: GS (satellite gliall cells, SGC), GFAP (activated SGC), ED-1 (activated macrophages), Ki67 (proliferating cells), TNFa and IL-6 and their receptors (pro-inflammatory cytokines), SOCS3 (supressor of cytokine signalling), STAT3 (transcription activator), TLR4 (membrane receptor implicated in induction of neuropathic pain) and COX2 (enzym implicated in inflammation). Only small weak of GFAP positive satellite cells cells were observed in DRG of naive rats, but their number was markedly increased in animals surviving 3 and especially 7 days. Double immunofluorescence staining with Ki67 and GS showed only scattered proliferating cells including a small number of SGC. The activation of SGC was associated with expression of TNFa and IL-6 and their receptors in neurons of the small and medium size as in hypertrophic SGC around large neurons. In comparison to naive rats, the ED-1 and SOCS3 immunostaining was decreased whereas the STAT3 was increased in DRG of Paclitaxel treated rats. No significant increase TLR4 and COX2 was also observed in comparison with naive DRG. Our results provide evidence on inflammatory reactions in DRG of Paclitaxe-treated rats that differ from neuropathic pain models based on nerve injury. |
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