Fuat Uslusoy1, Mustafa Nazıroğlu2,3, Kemal Ertilav4. 1. Department of Plastic Reconstructive and Aesthetic Surgery, Faculty of Medicine, Suleyman Demirel University Isparta, Turkey. 2. Neuroscience Research Center, Suleyman Demirel University Isparta, Turkey. 3. Drug Discovery Unit, BSN Health, Analyses, Innovation, Consultancy, Organization, Agriculture and Industry Ltd Göller Bölgesi Teknokenti, Isparta, Turkey. 4. Departmant of Neurosurgery, Faculty of Medicine, Suleyman Demirel University Isparta, Turkey.
Abstract
BACKGROUND: Mechanical sciatic nerve (MSN) injury has a high rate within trauma cases. Heat and cold exposure in the treatments of MSN injuries have been clinically used in human. The MSN injury results in apoptosis, overload Ca2+ influx, and reactive oxygen species (ROS) generation in the sciatic nerve. TRPM2 and TRPM8 cation channels are activated by ROS. TRPM2 is activated by warmth (36-38°C) and heat (45-47°C), although TRPM8 is activated by cold (0-25°C). Heat or cold exposure may aid recovery MSN injury through modulation of TRPM2 and TRPM8 in sciatic nerve. OBJECTIVE: The protective roles of cold and heat treatments via modulation of TRPM2 and TRPM8 were evaluated on MSN injury-induced neurotoxicity in in vitro models of mouse and the SH-SY5Y cell line. METHOD: The mice sciatic nerves and SH-SY5Y cells were divided into control (37°C), cold (10°C), and moderate heat (40°C) groups. RESULTS: Our data identified a decrease in injury diameter in the neurons following heat exposure, but not cold exposure. In addition, the results of laser confocal microscopy analyses were indicative of a protective role of TRPM8 antagonist (ACA) against cold-induced increases in Ca2+ influx in the sciatic nerve and TRPM8 expressing SH-SY5Y cells. The results of the automatic plate reader and laser confocal microscope assays indicated a protective role of heat treatment against MSN injury-induced increases in apoptosis, mitochondrial ROS, cytosolic ROS, caspase -3, and -9 in the neurons. CONCLUSIONS: The heat treatment via possible modulation of TRPM2 channel and heat shock proteins induced protective actions against injury-mediated increases of oxidative stress, excitotoxicity, and apoptosis in the sciatic nerve and SH-SY5Y cells. IJBT
BACKGROUND: Mechanical sciatic nerve (MSN) injury has a high rate within trauma cases. Heat and cold exposure in the treatments of MSN injuries have been clinically used in human. The MSN injury results in apoptosis, overload Ca2+ influx, and reactive oxygen species (ROS) generation in the sciatic nerve. TRPM2 and TRPM8 cation channels are activated by ROS. TRPM2 is activated by warmth (36-38°C) and heat (45-47°C), although TRPM8 is activated by cold (0-25°C). Heat or cold exposure may aid recovery MSN injury through modulation of TRPM2 and TRPM8 in sciatic nerve. OBJECTIVE: The protective roles of cold and heat treatments via modulation of TRPM2 and TRPM8 were evaluated on MSN injury-induced neurotoxicity in in vitro models of mouse and the SH-SY5Y cell line. METHOD: The mice sciatic nerves and SH-SY5Y cells were divided into control (37°C), cold (10°C), and moderate heat (40°C) groups. RESULTS: Our data identified a decrease in injury diameter in the neurons following heat exposure, but not cold exposure. In addition, the results of laser confocal microscopy analyses were indicative of a protective role of TRPM8 antagonist (ACA) against cold-induced increases in Ca2+ influx in the sciatic nerve and TRPM8 expressing SH-SY5Y cells. The results of the automatic plate reader and laser confocal microscope assays indicated a protective role of heat treatment against MSN injury-induced increases in apoptosis, mitochondrial ROS, cytosolic ROS, caspase -3, and -9 in the neurons. CONCLUSIONS: The heat treatment via possible modulation of TRPM2 channel and heat shock proteins induced protective actions against injury-mediated increases of oxidative stress, excitotoxicity, and apoptosis in the sciatic nerve and SH-SY5Y cells. IJBT