Institution
Liaoning University of Traditional Chinese Medicine
Education•Shenyang, China•
About: Liaoning University of Traditional Chinese Medicine is a education organization based out in Shenyang, China. It is known for research contribution in the topics: Randomized controlled trial & Acupuncture. The organization has 2040 authors who have published 1326 publications receiving 14664 citations.
Topics: Randomized controlled trial, Acupuncture, Apoptosis, Cancer, Portulaca
Papers published on a yearly basis
Papers
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TL;DR: The results show that acupuncture can alleviate the myocardial ischemia of cardiac tissue, decrease significantly the activities of serum SOD and MDA, and thereby influence the protein expressions of CFTR and CLC-2 in CL− channels.
Abstract: Recent evidence suggests that chloride (CL−) channels are involved in myocardial ischemia. In this study, the impact of acupuncture on the protein expressions of Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) and CLC-2 CL− channel of the rats with myocardial ischemia were tested and its mechanism was explored. The rats for experiment were distributed randomly into 5 groups: blank control group, modeling control group, Neiguan (PC-6) treatment group, Lieque (LU-7) control group, and Non-acupoint control group. The rats of all groups, except the blank control group, had myocardial ischemia via multiple subcutaneous injection of isoproterenol (ISO). Electroacupuncture treatment was given to Neiguan (PC-6) treatment group, Lieque (LU-7) control group, and Non-acupoints control group, respectively, once a day for 7 days. The results show that acupuncture can alleviate the myocardial ischemia of cardiac tissue, decrease significantly the activities of serum SOD and MDA, and thereby influence the protein expressions of CFTR and CLC-2 in CL− channels. The results of the study implies that acupuncture suppresses the pathological changes of cardiac tissue of rats with myocardial ischemia and regulates the protein expression of CFTR and CLC-2 CL− channels, which may serve as one possible mechanism to reduce myocardial ischemia.
9 citations
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TL;DR: Cardiac-specific LonP1 deficiency causes aberrant metabolic reprogramming of cardiomyocytes, pathological heart remodeling, as well as impeded heart function, which offers exciting new insights into the potential therapeutic strategy for heart failure.
Abstract: Protein quality control is pivotal to cellular homeostasis and integrity of cardiomyocytes for maintenance of normal heart function. The unfolded protein response (UPR) is an adaptive process to modulate protein quality control in the endoplasmic reticulum (ER) and mitochondria, and is accordingly termed UPRER and UPRmt, respectively. Lon protease (LonP1) is a highly conserved mitochondrial protease to modulate UPRmt, which is involved in regulating metabolism, mitophagy, and stress response. However, whether LonP1 regulates UPRER remains elusive. To investigate the regulation of protein quality control in cardiomyocytes, we generated cardiac-specific LonP1 deletion mice. Our findings show that LonP1 deficiency caused impaired mitochondrial respiratory function and fragmentation. Surprisingly, both UPRER and UPRmt is substantially induced in LonP1-deletion heart suggesting of LonP1 as a novel regulator of UPRER; however, the activation of UPRER occurs earlier than UPRmt in response to LonP1 deletion. Consequently, cardiac-specific LonP1 deficiency causes aberrant metabolic reprogramming of cardiomyocytes, pathological heart remodeling, as well as impeded heart function. Thus, we uncovered the novel function of LonP1 as an UPRmt mediator, and reciprocal orchestration of UPRmt and UPRER and mitochondrial dynamics regulated by LonP1 in the cardiomyocytes that is critical to maintain heart function, which offers exciting new insights into the potential therapeutic strategy for heart failure.
9 citations
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TL;DR: This systematic review will provide an evidence of CHFs composed under the guidance by 3 TCM treatment methods with routine drugs, compared withoutine drugs alone for IPF, and will submit to a peer-reviewed journal for publication.
9 citations
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TL;DR: TIIA can lower levels of serum lipids, stabilize atherosclerotic plaques, reduce endothelial injury, and inflammatory damage by activation of the TGF-β/PI3K/Akt/eNOS pathway.
Abstract: Objective Explored the mechanism of action of tanshinone IIA (TIIA) against atherosclerosis. Methods ApoE mice were divided into two groups of 10: model and TIIA. A control group of 10 wild-type mice was created. ApoE mice were fed a high-fat diet for 12 weeks. The TIIA group received TIIA once daily. Mice were anesthetized, blood collected by cardiac puncture, and the aortic sinus/arch collected for histology and molecular studies, respectively. Results Mice intima in the model group had large areas of plaque formation, serum levels of total cholesterol (TC), triglycerides, and low-density lipoprotein-cholesterol (LDL-C) increased significantly, and high-density lipoprotein-cholesterol (HDL-C) levels decreased significantly in the model group after 12 weeks. Staining [hematoxylin and eosin (H&E), Oil-Red-O] showed that the aorta had lesions, a higher degree of plaque formation, and considerable lipid deposition in model-group mice. After TIIA treatment, expression of HDL-C was increased significantly and that of TC, triglycerides and LDL-C decreased significantly, and plaque size and lipid deposition improved obviously. Analyses of protein phosphorylation in aortic tissue suggested that the transforming growth factor (TGF)-β/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/endothelial nitric oxide synthase (eNOS) pathway was activated in TIIA-treated mice. Conclusion TIIA can lower levels of serum lipids, stabilize atherosclerotic plaques, reduce endothelial injury, and inflammatory damage by activation of the TGF-β/PI3K/Akt/eNOS pathway.
9 citations
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TL;DR: The affecting factors and key problems in toxicity attenuation of fleece-flower root are discussed on the basis of sorting out the processing methods in ancient medical books and modern standards, in order to provide the reference for establishing specification for toxicity attenuations of fleee-flowerroot.
Abstract: In recent years, the rapid growth of reports on fleece-flower root-caused liver damages has drawn wide attention of both at home and abroad, however, there were rare literature on toxicology of fleece-flower root in ancient Chinese medicine. But why there are so many reports on toxicology of fleece-flower root now compared with the ancient literature? As a typical tonic medicine, the clinical utility of fleece-flower root was largely limited by its standardization and reliability of processing methods in ancient Chinese medicine. The ancient processing methods of fleece-flower root emphasized nine times of steaming and nine times of drying, while the modern processes have been simplified into one time of steaming. Whether the differences between ancient and modern processing methods are the potential cause of the increased events of fleece-flower root-caused liver damages. We will make deep analysis and provide new clues and perspectives for the research on its toxicity. This article, therefore, would discuss the affecting factors and key problems in toxicity attenuation of fleece-flower root on the basis of sorting out the processing methods of fleece-flower root in ancient medical books and modern standards, in order to provide the reference for establishing specification for toxicity attenuation of fleece-flower root.
9 citations
Authors
Showing all 2045 results
Name | H-index | Papers | Citations |
---|---|---|---|
Hang Xiao | 64 | 618 | 16026 |
Muhammad Riaz | 58 | 934 | 15927 |
Jianping Liu | 45 | 333 | 7977 |
Guoan Luo | 45 | 221 | 6358 |
Xingshun Qi | 40 | 308 | 5409 |
Mei Wang | 29 | 201 | 6007 |
Xiaozhong Guo | 28 | 142 | 2269 |
Zhiwei Cao | 27 | 110 | 2879 |
Xinggang Yang | 26 | 113 | 2292 |
Ruixin Zhu | 25 | 110 | 2119 |
Ran Wang | 23 | 157 | 1942 |
Li-Ping Bai | 22 | 95 | 1824 |
Ke Liu | 19 | 31 | 1183 |
Ahmed M. Metwaly | 17 | 51 | 682 |
Kailin Tang | 17 | 40 | 919 |