Tissue & cell · 2025
Neuroprotective effects of granulocyte colony-stimulating factor against tramadol-induced cerebellar neurotoxicity.
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Attia Ghalia Mahfouz, Ali Lashin S, Eldesoqui Mamdouh, Elsaed Wael M, Mostafa Sally Abdallah, Albadawi Emad A, Elmansy Rasha Ahmed, Elhassan Yasir Hassan, Berika Mohamed, Badawy Abdelnaser A, El-Nabalaway Mohammad, Dawood Amal Fahmy, Seleem Hanan Said
Аннотация
BACKGROUND: Tramadol (TRM) is a centrally acting synthetic opioid and serotonin/norepinephrine reuptake inhibitor. Despite being a potent painkiller, long-term use can induce permanent neurotoxicity. Granulocyte colony-stimulating factor (G-CSF) is a cytokine that helps to mobilize stem cells and facilitate their integration over injured neurons.
AIM: This work aims to study the histopathological, biochemical, and molecular alterations in the cerebellar cortex induced by TRM in comparison to the postulated protective effect of G-CSF versus TRM withdrawal.
METHODS: 32 adult male albino rats were equally divided into four groups: control, TRM, TRM+G-CSF-treated, and TRM withdrawal groups. The TRM group received a daily dose of 80 mg/kg body weight orally via gastric tube for 12 weeks. The TRM+G-CSF-treated group received subcutaneous injections of 100 μg/kg body weight of G-CSF for seven consecutive days, then TRM from the 8th day. The TRM withdrawal group received TRM for 12 weeks; then, the rats were left without TRM administration for a further 12 weeks. The structural, biochemical, and molecular changes of the cerebellum were measured.
RESULTS: The study revealed that TRM not only induced cerebellar atrophy but also triggered microgliosis, neuroinflammation, and apoptotic indicators, all while suppressing autophagy. However, G-CSF and TRM withdrawal reversed these alterations with superiority to G-CSF.
CONCLUSION: The current investigation shows that G-CSF may improve behavioral, neurochemical, immunohistochemical, and molecular metrics in the rat cerebellum after tramadol-induced injury. G-CSF exhibits a superior protective effect compared to tramadol withdrawal. This is achieved through its antioxidant, anti-apoptotic, and autophagic enhancement properties, as well as its ability to reduce cerebellar gliosis.
AIM: This work aims to study the histopathological, biochemical, and molecular alterations in the cerebellar cortex induced by TRM in comparison to the postulated protective effect of G-CSF versus TRM withdrawal.
METHODS: 32 adult male albino rats were equally divided into four groups: control, TRM, TRM+G-CSF-treated, and TRM withdrawal groups. The TRM group received a daily dose of 80 mg/kg body weight orally via gastric tube for 12 weeks. The TRM+G-CSF-treated group received subcutaneous injections of 100 μg/kg body weight of G-CSF for seven consecutive days, then TRM from the 8th day. The TRM withdrawal group received TRM for 12 weeks; then, the rats were left without TRM administration for a further 12 weeks. The structural, biochemical, and molecular changes of the cerebellum were measured.
RESULTS: The study revealed that TRM not only induced cerebellar atrophy but also triggered microgliosis, neuroinflammation, and apoptotic indicators, all while suppressing autophagy. However, G-CSF and TRM withdrawal reversed these alterations with superiority to G-CSF.
CONCLUSION: The current investigation shows that G-CSF may improve behavioral, neurochemical, immunohistochemical, and molecular metrics in the rat cerebellum after tramadol-induced injury. G-CSF exhibits a superior protective effect compared to tramadol withdrawal. This is achieved through its antioxidant, anti-apoptotic, and autophagic enhancement properties, as well as its ability to reduce cerebellar gliosis.