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Wiad Lek ; 76(2): 326-331, 2023.
Article in English | MEDLINE | ID: mdl-37010169

ABSTRACT

OBJECTIVE: The aim: The purpose of the research was to study the role of infiximab global cerebral ischemia-reperfusion injury. PATIENTS AND METHODS: Materials and methods: The rats were split into five groups: Sham group; Control group: occlusion of the common carotid artery for 60 minutes, and sub-sequently reperfusion for an hour without receiving any medication; Vehicle group: as the control group, but 72 hours before to the ischemia, they were given the medication 0.9 NaCl intraperitoneally (i.p); Treated group-1: as the control group, plus 3 mg/kg of IFX intraperitoneally (i.p) 72 hours prior to ischemia; Treated group-2: as the control group, plus 7 mg/kg of IFX intraperitoneally (i.p) 72 hours prior to ischemia. RESULTS: Results: Pre-treatment with IFX significantly reduced the percentage of infarct area, but in the IFX (7 mg/kg) group, the infarct area was smaller than at the low dose. The ischemia group had a significant elevated of TNF- α and caspase-3 while a significant lowered in CAT and SOD levels. The pre-treatment with IFX, the TNF- α and caspase-3 levels lowered significantly, furthermore, significantly increased CAT and SOD levels activity (P≤0.05) as compared with IR group. Among effective groups, I/R+IFX (7mg/kg) group more effective in lowering TNF- α and caspase than I/R+IFX (3mg/kg) group. CONCLUSION: Conclusions: Infiximab has neuroprotective effective due to its powerful TNF- α blocker and limit ROS release and cell death signaling which protects the neurons from injury during cerebral ischemia reperfusion.


Subject(s)
Brain Ischemia , Cerebral Infarction , Humans , Infliximab/pharmacology , Infliximab/therapeutic use , Caspase 3/pharmacology , Caspase 3/therapeutic use , Cerebral Infarction/drug therapy , Cerebral Infarction/etiology , Brain Ischemia/drug therapy , Apoptosis , Tumor Necrosis Factor-alpha , Reperfusion , Superoxide Dismutase
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