Effect of amifostine on apoptotic inflammatory makers in cisplatin induced brain damage in rats.

Objectives: To lessen the negative effects of the medication, we assessed the neuroprotective impact of amifostine nanoparticles against the neurotoxicity generated by cisplatin.

Methods: 60 adult male albino Wistar rats were arranged into six groups. Group 1; received saline intraperitonealy (IP) and served as negative control. Group 2; received IP injection of silica nano-emulsion, Group 3 received cispatin for three consecutive days at the end of the study, Group 4 received amifostine intrapretonealy (IP) before cisplatin injection, Group 5 received silica nano-emulsion alone for one month, group 6 received silica nano-emulsion in combination with cisplatin for three consecutive days at the end of the study. Monocyte chemoattractant protein-1 (MCP-1) and glial fibrillary acidic protein (GFAP) were estimated by ELISA, butrylcholinesterase (BChE) by spectrophotometric method while caspase-3 as a marker of apoptosis by PCR.

Results: The mean levels of brain GFAP, MCP-1, and caspase-3 in the cisplatin group were considerably higher than those in the control group. However, there was a drop in the average level of brain BChE activity. Additionally, the injection of (SiNPs@AMF + cisplatin) increased BChE activities while reducing GFAP, MCP-1, and caspase-3 levels, thereby reversing the negative effects of cisplatin on the brain tissue. On the other hand, the group treated with SiNPs@AMF + cisplatin showed improvement in overall brain structure and minimal pyknotic nuclei and apoptotic neurons were found.

Conclusions: These outcomes demonstrated amifostine's ability to lessen the histological changes brought on by cisplatin. To sum up, SiNPs@AMF may be a suitable and secure supplemental treatment agent to lessen cisplatin's toxicity in the brain and enhance the treatment's effects throughout chemotherapy.