OBJECTIVE: To observe MMP9 expression in rat lungs under different degrees of hyperbaric oxygen (HBO2) exposure and to observe the relationship of tissue damage and apoptosis rate in the lung tissue. METHODS: 40 Sprague Dawley (SD) rats were randomly divided into five groups: 250 kPa oxygen exposure for two-, four-, six- and eight-hour exposures and a "normal group," each n = 8. After hyperbaric oxygen treatment, the rats were euthanized immediately to collect lung tissue. We used HE staining to detect the pathological changes and immunohistochemistry to detect in situ expression of matrix metalloproteinase 9 (MMP9). Then we tested the expression level of caspase 3 in lung tissue by Western Blot. To understand the antioxidant capacity changes, we detected superoxide dismutase (SOD) activities and malondialdehyde (MDA) contents in lung tissue during HBO2 exposure. Finally, we exposed MMP9 knockout or wild-type mice under hyperbaric oxygen for six hours, and detected the pathological changes with HE staining. RESULT: Lung tissue damage changed gradually under different degrees of hyperbaric oxygen exposure, but eased in the six-hour group. However, MMP9 expression decreased initially and then was upregulated until it reached the peak after six hours of exposure; it then reduced significantly after an eight-hour exposure. Active caspase 3 reached the highest level after eight hours. While SOD activity was upregulated only after six hours of HBO2 exposure, MDA content increased after eight hours of exposure. CONCLUSIONS: MMP9 expression was elevated after exposure to hyperbaric oxygen. This is a compensatory mechanism of the body's antioxidant response by regulating the inflammatory response. This in turn helps to reduce the apoptosis rate and protects lung tissue from oxygen toxicity.
OBJECTIVE: To observe MMP9 expression in rat lungs under different degrees of hyperbaric oxygen (HBO2) exposure and to observe the relationship of tissue damage and apoptosis rate in the lung tissue. METHODS: 40 Sprague Dawley (SD) rats were randomly divided into five groups: 250 kPa oxygen exposure for two-, four-, six- and eight-hour exposures and a "normal group," each n = 8. After hyperbaric oxygen treatment, the rats were euthanized immediately to collect lung tissue. We used HE staining to detect the pathological changes and immunohistochemistry to detect in situ expression of matrix metalloproteinase 9 (MMP9). Then we tested the expression level of caspase 3 in lung tissue by Western Blot. To understand the antioxidant capacity changes, we detected superoxide dismutase (SOD) activities and malondialdehyde (MDA) contents in lung tissue during HBO2 exposure. Finally, we exposed MMP9 knockout or wild-type mice under hyperbaric oxygen for six hours, and detected the pathological changes with HE staining. RESULT: Lung tissue damage changed gradually under different degrees of hyperbaric oxygen exposure, but eased in the six-hour group. However, MMP9 expression decreased initially and then was upregulated until it reached the peak after six hours of exposure; it then reduced significantly after an eight-hour exposure. Active caspase 3 reached the highest level after eight hours. While SOD activity was upregulated only after six hours of HBO2 exposure, MDA content increased after eight hours of exposure. CONCLUSIONS:MMP9 expression was elevated after exposure to hyperbaric oxygen. This is a compensatory mechanism of the body's antioxidant response by regulating the inflammatory response. This in turn helps to reduce the apoptosis rate and protects lung tissue from oxygentoxicity.