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Liu S.-R.,Liaoning Medical University | Yu B.,The First Peoples Hospital of Shenyang City | Jiao B.-P.,Liaoning Medical University | Liu Y.-F.,Liaoning Medical University
Chinese Journal of Tissue Engineering Research

Background: How to control functional activity of donor liver after cardiac death and maintain the optimal function of grafts are the key issues in organ transplantation study. Objective: To preliminarily explore the effect of warm ischemia injury on the morphology and function of rat donor liver after cardiac death. Methods: Cardiac death model was established in Sprague-Dawley rats and the successful models were divided into six groups: control group (warm ischemia for 0 minute), warm ischemia 10 group (warm ischemia for 10 minutes), warm ischemia 20 group (warm ischemia for 20 minutes), warm ischemia 30 group (warm ischemia for 30 minutes), warm ischemia 40 group (warm ischemia for 40 minutes) and warm ischemia 50 group (warm ischemia for 50 minutes). The rat liver specimens in each group were cut into ultrathin sections. The structure of liver cells was observed and photographed by electron microscopy. Flameng score was applied to analyze the degree of mitochondrial damage. Liver mitochondria were extracted and then spectrophotometry was used to assess the viability of cytochrome C oxidase. Results and Conclusion: Under electron microscopy, there were no significant changes in liver cells within 30 minutes of warm ischemia, nuclear membrane was intact, mitochondria mildly swelled, no mitochondrial crista ruptured, and Flameng score was < 2 points. With the extension of warm ischemia time, the cells became swelling, nuclear chromatin condensated, apoptotic body was clearly visible, mitochondrial matrix coagulated, mitochondria exhibited vacuolation, and Flameng score was 3-4 points. The viability of cytochrome C oxidase showed no significant difference within 30 minutes of warm ischemia, but began to significantly decrease at 40 and 50 minutes. The mitochondrial structure and function after liver injury is not obviously affected by 30 minutes of warm ischemia, and significant changes appear after 40 minutes. Source

Zhang X.,Nanjing Medical University | Hu W.,Nanjing Medical University | Wu F.,The First Peoples Hospital of Shenyang City | Yuan X.,The First Peoples Hospital of Shenyang City | Hu J.,Nanjing Medical University
Canadian Journal of Physiology and Pharmacology

Shikonin is a naphthoquinone compound extracted from the Chinese herb purple gromwell. Shikonin has broad antibacterial, anti-inflammatory, and antitumor activities. The tumor necrosis factor-α (TNF-α)-induced proliferation and invasion of vascular smooth muscle cells (VSMCs) is an important factor that contributes to atherosclerosis. The effects of shikonin on the proliferation and apoptosis of VSMCs have been reported; however, the function of shikonin on TNF-α-mediated growth and invasion of VSMCs during atherosclerosis remains unclear. In this study, we used Western blot, flow cytometry, real-time quantitative PCR, and enzyme-linked immunosorbent assay to investigate the effect of shikonin on the TNF-α-induced growth and invasion of VSMCs and to determine the underlying mechanism. Our results showed that shikonin inhibits the TNF-α-mediated growth and invasion. Further study revealed that shikonin regulates the activation of nuclear factor kappa B and phosphatidyl inositol 3-kinase signaling pathways; modulates the expression of cyclin D1, cyclin E, B-cell lymphoma 2, and Bax; activates caspase-3 and caspase-9; induces cell cycle arrest; and promotes the apoptosis of VSMCs. Together, our results indicate that shikonin may become a promising agent for the treatment of atherosclerosis and they also establish foundation for the development of anti-atherosclerosis drugs. © 2015, National Research Council of Canada. All Rights Reserved. Source

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