cellular
• reduced apoptosis after LPS injection
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• reduced apoptosis upon LPS stimulation of renal tubular epithelial cells (RTECs)
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homeostasis/metabolism
• no increase in intra- or extracellular hydrogen peroxide generation upon LPS stimulation of renal tubular epithelial cells (RTECs)
• suppressed extracellular hydrogen peroxide generation by kidneys after LPS injection
• attenuated TNFA and IL1b induction upon LPS stimulation of renal tubular epithelial cells (RTECs)
• no TNFA and IL1b production by kidneys after LPS injection
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immune system
• attenuated IL1b induction upon LPS stimulation of renal tubular epithelial cells (RTECs)
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• attenuated TNFA induction upon LPS stimulation of renal tubular epithelial cells (RTECs)
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• significantly increased survival rate after LPS injection
• no increase in intra- or extracellular hydrogen peroxide generation upon LPS stimulation of renal tubular epithelial cells (RTECs)
• suppressed extracellular hydrogen peroxide generation by kidneys after LPS injection
• attenuated TNFA and IL1b induction upon LPS stimulation of renal tubular epithelial cells (RTECs)
• no TNFA and IL1b production by kidneys after LPS injection
• no acute kidney injury (AKI) after LPS injection
• suppressed macrophage and neutrophil infiltration of kidney after LPS induction
• reduced kidney apoptosis after LPS injection
• no glomerular swelling after LPS injection
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mortality/aging
• significantly increased survival rate after LPS injection
• no acute kidney injury (AKI) after LPS injection
• suppressed macrophage and neutrophil infiltration of kidney after LPS induction
• reduced kidney apoptosis after LPS injection
• no glomerular swelling after LPS injection
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renal/urinary system
• reduced apoptosis after LPS injection
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• reduced apoptosis upon LPS stimulation of renal tubular epithelial cells (RTECs)
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