| Summary: | 碩士 === 國立交通大學 === 生物科技學系 === 104 === Acute kidney injury (AKI) is a serious complication of systemic inflammatory response syndrome. Although therapy for AKI has improved in recent years, AKI is still highly prevalent, especially in critically ill patients in the intensive care unit (ICU). AKI in the ICU has high mortality rates, reaching 80%. Tauroursodeoxycholic Acid (TUDCA) is recently found to suppress lipopolysaccharide (LPS) - induced acute kidney injury. We studied the mechanism of the mice injection LPS cause acute kidney injury.
Mice distributed into three groups. First group was control. The second group were injected with LPS (8 mg/kg). The third group were injected TUDCA (500 mg/kg) before LPS injection. Mice LPS-injection after 48 hours, mice sacrificed and collected blood and tissues.
Mice LPS-injection after 48 hours, we detected serum glucose, triglyceride, and cholesterol to success LPS-induced acute kidney injury. We isolated mice kidney mRNA and protein. LPS-injected mice were increased ER stress marker BIP and CHOP expression, inflammatory cytokines TNF-α and IL-6 expression, and mitochondrial fission marker DRP1 and FIS1 expression. Mitochondrial fusion marker MFN1, MFN2, and OPA1 were no significant difference. TUDCA treatment suppressed this changes. LPS-induced acute kidney injury was associated with vacuolar degeneration and apoptosis of renal tubular cells. Injection TUDCA ameliorated LPS-induced acute kidney injury in WT mice and apoE mice.
LPS modulate acute kidney injury through enhanced ER stress and mitochondrial dynamic.
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