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Neuroprotective effects of methane-rich saline on experimental acute carbon monoxide toxicity.
Journal of the Neurological Sciences 2016 October 16
BACKGROUND: Methane has been reported to play a protective role in ischemia-reperfusion injury via anti-oxidation, anti-inflammatory and anti-apoptotic activities. This study was designed to determine the protective effects of methane-rich saline (MRS) on acute carbon monoxide (CO) poisoning.
METHODS: A total of 36 male Sprague-Dawley rats were randomly divided into 3 groups: sham group, CO group and MRS group. Acute CO poisoning was induced by exposing rats to 1000ppm CO in air for 40min and then to 3000ppm CO for an additional 20min until they lost consciousness. MRS at 10ml/kg was intraperitoneally administered at 0h, 8h and 16h after CO exposure. Rats were sacrificed 24h after CO exposure. Brains were collected for Nissl staining. The cortex and hippocampus were separated for the detections of malondialdehyde (MDA), 3-nitrotyrosine (3-NT), 8-hydroxydeoxyguanosine (8-OHdG), tumor necrosis factor-α (TNF-α), interleukin1-β (IL-1β), interleukin-6 (IL-6) and superoxide dismutase (SOD) activities.
RESULTS: The results showed that MRS treatment improved neuronal injury, reduced MDA, 3-NT and 8-OHdG, and increased SOD activity of the hippocampus and cortex compared with normal saline-treated rats. In addition, MRS reduced the expression of TNF-α and IL-1β in the brain but had no effect on IL-6 expression.
CONCLUSION: These findings suggest that MRS may protect the brain against acute CO poisoning-induced injury via its anti-oxidative and anti-inflammatory activities.
METHODS: A total of 36 male Sprague-Dawley rats were randomly divided into 3 groups: sham group, CO group and MRS group. Acute CO poisoning was induced by exposing rats to 1000ppm CO in air for 40min and then to 3000ppm CO for an additional 20min until they lost consciousness. MRS at 10ml/kg was intraperitoneally administered at 0h, 8h and 16h after CO exposure. Rats were sacrificed 24h after CO exposure. Brains were collected for Nissl staining. The cortex and hippocampus were separated for the detections of malondialdehyde (MDA), 3-nitrotyrosine (3-NT), 8-hydroxydeoxyguanosine (8-OHdG), tumor necrosis factor-α (TNF-α), interleukin1-β (IL-1β), interleukin-6 (IL-6) and superoxide dismutase (SOD) activities.
RESULTS: The results showed that MRS treatment improved neuronal injury, reduced MDA, 3-NT and 8-OHdG, and increased SOD activity of the hippocampus and cortex compared with normal saline-treated rats. In addition, MRS reduced the expression of TNF-α and IL-1β in the brain but had no effect on IL-6 expression.
CONCLUSION: These findings suggest that MRS may protect the brain against acute CO poisoning-induced injury via its anti-oxidative and anti-inflammatory activities.
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