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

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

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.

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.

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.