cellular
N |
• normal reactive oxygen species (ROS) generation increase upon stimulation of smooth muscle cells (SMCs) with TLR2 agonist Pam3CSK4 or PMA stimulation of bone marrow-derived monocytes
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• 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
|
immune system
• attenuated IL1b induction upon LPS stimulation of renal tubular epithelial cells (RTECs)
|
• attenuated TNFA induction upon LPS stimulation of renal tubular epithelial cells (RTECs)
|
• 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
|
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
|
renal/urinary system
• reduced apoptosis after LPS injection
|
• reduced apoptosis upon LPS stimulation of renal tubular epithelial cells (RTECs)
|