J Exp Clin Neurosci, 2019, 6(1): 1-5 1 Original Artcle Cerebrolysin Ameliorates Cisplatin-Induced Neuropathic Pain in Mice: A Behavioral Study Ali Namvaran-Abbas-Abad a , Fereshteh Farajdokht b , Saeed Sadigh-Eteghad b , Javad Mahmoudi b , Seyed Mahdi Vatandoost b, * a Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran b Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran Introduction Neuropathic pain is a chronic pain condition affecting millions of individuals worldwide [1]. This condition is caused by different ailments, such as diabetes [2], injuries, and interventions [3-5], that affect the somatosensory system [1]. Chronic pain results in a great many of these cases [6]. Chemotherapy-induced peripheral neuropathy (CIPN) is a troublesome chronic condition experienced by 30% to 40 % of patients undergoing sequential chemotherapy, and it remains as a common dose-limiting side effect of chemotherapeutic agents [3, 7]. Moreover, CIPN may have negative consequences on treatment procedures [8], quality of life, and daily activities [3, 7, 8]. Unfortunately, little is known about CIPN’ss exact pathophysiology, and available treatments have a restricted effciency in relieving pain [8]. Cisplatin is a potent chemotherapeutic agent used to treat a wide range of solid tumors, including testicular, ovarian, and bladder cancers [9]. The aadministration of cisplatin is also associated with neurotoxicity via irreversible axonal loss [10] and with neuropathic pain in distal extremities [11]. Cisplatin is extensively used as an animal model of neuropathy pain to study the effects of neuroprotective substances [11-13]. However, pain management remains a major challenge that restricts cisplatin use in clinical settings. In addition, currently available therapies are not able to effectively control neuropathic pain symptoms [11, 14]. Cerebrolysin (CBL) is a purifed mixture containing a fraction of free amino acids and some brain growth factors [15], including brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF), nerve growth factor (NGF), and ciliary neurotrophic factor (CNTF) [16]. Evidence shows that CBL is capable of partially crossing the blood-brain barrier because it contains low molecular weight peptides. Previous research has shown that CBL improves different neurological conditions, Abstract Objectve: Cisplatn (Cis) is a potent chemotherapeutc agent in clinical use which is associated with nephrotoxicity and neuropathic pain possibly through infammatory response. Cerebrolysin (CBL), a mixture of neurotrophins, has analgesic and ant-infammatory propertes. The aim of the present study was to investgate the efects of cerebrolysin on cisplatn-induced neuropathic pain in mice. Materials and Methods: Mice were randomly divided into fve groups: Control, Cis, Cis + CBL, Cis + Vitamin E (Vit E), and Cis + Morphine. CBL and Vit E were injected for four consecutve days following a single injecton of Cis. On day 4, the mice were subjected to three behavioral tests: cold plate, hot plate, and formalin. Results: The results showed that mice treated with CBL had higher withdrawal thresholds for both the hot plate and cold plate tests and displayed lower hyperalgesia-related behaviors for the formalin test compared to the Cis group. Moreover, CBL induced higher ant-nociceptve efects than Vit E and lesser efects than morphine in both hot plate and cold plate tests. Furthermore, the analgesic efect of CBL was similar to the morphine efect in the late phase of the formalin test. Conclusion: These results indicate that CBL has an ant-nociceptve efect against cisplatn-induced neuropathic pain. Keywords: Cisplatn, Neuropathic Pain, Cerebrolysin, Hyperalgesia ©2019 Swedish Science Pioneers, All rights reserved. Correspondence Seyed Mahdi Vatandoust Neurosciences research center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran. Tel/Fax: +984133340730. Email: sm.vatandoust@gmail.com Received: 2018-10-10 Accepted: 2018-11-01 DOI:10.13183/jecns.v6i1.85