Investigation of NAS (N-acetiylycsteıne) effects on asprosin immunoreactivity in liver tissues of experimental methotrexate-treated rats

A folic acid antagonist, Methotrexate (MTX), is a cytotoxic chemotherapeutic agent used in the treatment of various diseases. Although widely used, its use is limited as it has serious side effects on tissues and organs. This study aimed to investigate both the effects of N-acetylcysteine (NAS), a potent antioxidant compound against MTX - induced liver injury, and to determine whether or not a newly discovered adipokine, Asprosin, changes in serum and tissue due to MTX-induced damage. In this study 8-10 weeks aged, twenty-four male Wistar Albino rats were used. The experimental animals used were divided into 4 groups of 6 animals in each group.No treatment was applied to the control group during the 14 days of experimental period. 100 mg / kg / day N-NAS was administered intraperitoneally (i.p.) to the NAS group. MTX group received a single dose of ( i.p) 20mg / kg methotrexate. MTX+NAS group received a single dose of ( i.p) 20mg / kg methotrexate with 100 mg / kg / day NAS . Rats in all groups were decapitated under anesthesia at the end of 14 days of experimental period and tissue and blood samples were taken. Tissues were embedded in paraffin blocks through routine histological follow-up series. TUNEL method for apoptosis and avidin-biotin-peroxidase method for asprosin immunoreactivity were applied to the sections taken from paraffin blocks. In this study, no significant differences were observed between NAC and Control group in terms of analysed parameters. Compared with the control group, both TAS and asprosin levels decreased significantly while TOS levels increased in MTX group. In Comparision with the MTX group, a significantly decreased TOS levels and increased asprosin levels were observed in MTX+NAC group. As a result of MTX-induced toxicity, We observed that the liver TOS level increased while the asporsin level decreased. On the other hand NAC administration improved liver injury by decreasing the TOS level and increasing the asporsin level. We concluded that further experimental studies involving the treatment of MTX at different doses and durations are needed to clarify the effects of asprosin on the pathophysiology of liver tissue injury.