| Summary: | 博士 === 高雄醫學大學 === 天然藥物研究所 === 102 === Ischemia-reperfusion-elicited tissue injury contributes to morbidity and mortality in a wide variety of pathologies, including different organic injury in ascending order ischemia, infarction, and then organic failure. Acute hepatic ischemia-reperfusion (IR) injury is a common clinical problem and reactive oxygen species (ROS) may be a contributing factor on IR injury. Safflower is a popular folk medicine, but its activity on ischemia-reperfusion is rarely researched. The aim of this study was to evaluate the potential protective effect of safflower ethanol extract (SEE) on hepatic IR injury in a rat model. Caspases 3 and terminal deoxynucleotidyl transferase-mediated dUTP biotin nick end labeling (TUNEL) results showed increased cell death in the IR samples; reversely, minor apoptosis was detected in the SEE/IR group. Pretreatment with SEE significantly restored the content of antioxidant enzymes (SOD1 and catalase) and remarkably inhibited the intracellular ROS concentration in terms of reducing p47phox translocation. Proteome tools revealed that 20 proteins were significantly modulated in protein intensity between IR and SEE/IR groups. Particularly, SEE administration could attenuate the carbonylation levels of several chaperone proteins. Network analysis suggested that safflower extract could alleviate IR-induced endoplasmic reticulum (ER) stress and protein ubiquitination, which finally lead to cell apoptosis. Taken together, SEE could reduce hepatic IR injury through modulating protein oxidation and our results might help to develop novel therapeutic strategies against ROS-caused diseases.
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