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reuteri ) GMNL-263 prevented cardiac remodeling and inhibited the apoptosis of myocardial cells in NZB/WF1 mice, which were characterized by a decrease in the number of TUNEL-positive cells, related components of the Fas death receptor, and number of apoptotic cells in their heart tissues ( Table 1 )

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mechanism of action

As a result, the alveolar macrophage becomes profoundly deficient in glutathione and other anti-oxidants, and is therefore vulnerable to further cellular damage and dysfunction during the acute oxidative stress imposed by pneumonia or sepsis