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Your search keyword '"Liu, Rui"' showing total 19 results
Start Over Author "Liu, Rui" Journal biomed research international Publisher hindawi limited
19 results on '"Liu, Rui"'

9. Tilianin Protects against Ischemia/Reperfusion-Induced Myocardial Injury through the Inhibition of the Ca2+/Calmodulin-Dependent Protein Kinase II-Dependent Apoptotic and Inflammatory Signaling Pathways.

Author

Jiang, Hailun, Xing, Jianguo, Fang, Jiansong, Wang, Linlin, Wang, Yu, Zeng, Li, Li, Zhuorong, and Liu, Rui

Subjects
ANALYSIS of variance, APOPTOSIS, BIOLOGICAL assay, CELLULAR signal transduction, CORONARY disease, ENZYME-linked immunosorbent assay, FLAVONOIDS, HEART, INFLAMMATION, MOLECULAR structure, MYOCARDIAL reperfusion, DATA analysis software, PROTEIN kinase inhibitors, DESCRIPTIVE statistics
Abstract

Tilianin is a naturally occurring phenolic compound with a cardioprotective effect against myocardial ischemia/reperfusion injury (MIRI). The aim of our study was to determine the potential targets and mechanism of action of tilianin against cardiac injury induced by MIRI. An in silico docking model was used in this study for binding mode analysis between tilianin and Ca2+/calmodulin-dependent protein kinase II (CaMKII). Oxygen-glucose deprivation/reperfusion- (OGD/R-) injured H9c2 cardiomyocytes and ischemia/reperfusion- (I/R-) injured isolated rat hearts were developed as in vitro and ex vivo models, respectively, which were both treated with tilianin in the absence or presence of a specific CaMKII inhibitor KN93 for target verification and mechanistic exploration. Results demonstrated the ability of tilianin to facilitater the recovery of OGD/R-induced cardiomyocyte injury and the maintenance of cardiac function in I/R-injured hearts. Tilianin interacted with CaMKIIδ with an efficient binding performance, a favorable binding score, and restraining p-CaMKII and ox-CaMKII expression in cardiomyocytes injured by MIRI. Importantly, inhibition of CaMKII abolished tilianin-mediated recovery of OGD/R-induced cardiomyocyte injury and maintenance of cardiac function in I/R-injured hearts, accompanied by the disability to protect mitochondrial function. Furthermore, the protective effects of tilianin towards mitochondrion-associated proapoptotic and antiapoptotic protein counterbalance and c-Jun N-terminal kinase (JNK)/nuclear factor- (NF-) κB-related inflammation suppression were both abolished after pharmacological inhibition of CaMKII. Our investigation indicated that the inhibition of CaMKII-mediated mitochondrial apoptosis and JNK/NF-κB inflammation might be considered as a pivotal mechanism used by tilianin to exert its protective effects on MIRI cardiac damage. [ABSTRACT FROM AUTHOR]

Published
2020
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16. Lysophosphatidic Acid Inhibits Apoptosis Induced by Cisplatin in Cervical Cancer Cells

Author

Sui, Yanxia, primary, Yang, Ya, additional, Wang, Ji, additional, Li, Yi, additional, Ma, Hongbing, additional, Cai, Hui, additional, Liu, Xiaoping, additional, Zhang, Yong, additional, Wang, Shufeng, additional, Li, Zongfang, additional, Zhang, Xiaozhi, additional, Wang, Jiansheng, additional, Liu, Rui, additional, Yan, Yanli, additional, Xue, Chaofan, additional, Shi, Xiaowei, additional, Tan, Li, additional, and Ren, Juan, additional

Published
2015
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19. The Role of 99mTc-Annexin V Apoptosis Scintigraphy in Visualizing Early Stage Glucocorticoid-Induced Femoral Head Osteonecrosis in the Rabbit.

Author

Wang, Xiaolong, Liu, Yu, Wang, Xuemei, Liu, Rui, Li, Jianbo, Zhang, Guoliang, Li, Qiang, Wang, Lei, Bai, Zhigang, and Zhao, Jianmin

Subjects
ANIMAL experimentation, APOPTOSIS, OSTEONECROSIS, GLUCOCORTICOIDS, RABBITS, RADIONUCLIDE imaging, FEMUR head
Abstract

Objective. To validate the ability of 99mTc-Annexin V to visualize early stage of glucocorticoid-induced femoral head necrosis by comparing with 99mTc-MDP bone scanning. Methods. Femoral head necrosis was induced in adult New Zealand white rabbits by intramuscular injection of methylprednisolone. 99mTc-Annexin scintigraphy and 99mTc-MDP scans were performed before and 5, 6, and 8 weeks after methylprednisolone administration. Rabbits were sacrificed at various time points and conducted for TUNEL and H&E staining. Results. All methylprednisolone treated animals developed femoral head necrosis; at 8 weeks postinjection, destruction of bone structure was evident in H&E staining, and apoptosis was confirmed by the TUNEL assay. This was matched by 99mTc-Annexin V images, which showed a significant increase in signal over baseline. Serial 99mTc-Annexin V scans revealed that increased 99mTc-Annexin V uptake could be observed in 5 weeks. In contrast, there was no effect on 99mTc-MDP signal until 8 weeks. The TUNEL assay revealed that bone cell apoptosis occurred at 5 weeks. Conclusion. 99mTc-Annexin V is superior to 99mTc-MDP for the early detection of glucocorticoid-induced femoral head necrosis in the rabbit and may be a better strategy for the early detection of glucocorticoid-induced femoral head necrosis in patients. [ABSTRACT FROM AUTHOR]

Published
2016
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