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《医学前沿(英文)》 2023年 第17卷 第1期 页码 119-131 doi: 10.1007/s11684-022-0949-7
关键词: GDF15 esophageal squamous cell carcinoma chemoresistance cellular metabolism TGFBR2 AKT
LI Yanhua, BI Zhigang
《医学前沿(英文)》 2007年 第1卷 第1期 页码 79-86 doi: 10.1007/s11684-007-0016-4
Xiaoqing Li, Xinxin Li, Genbei Wang, Yan Xu, Yuanyuan Wang, Ruijia Hao, Xiaohui Ma
《医学前沿(英文)》 2018年 第12卷 第6期 页码 688-696 doi: 10.1007/s11684-018-0662-8
Xiao Ke Qing (XKQ) granule has been clinically used to treat type 2 diabetes mellitus (T2DM) for 10 years in Chinese traditional medication. However, its mechanisms against hyperglycemia remain poorly understood. This study aims to investigate XKQ mechanisms on diabetes and diabetic liver disease by using the KKAy mice model. Our results indicate that XKQ can significantly reduce food and water intake. XKQ treatment also remarkably decreases both the fasting blood glucose and blood glucose in the oral glucose tolerance test. Additionally, XKQ can significantly decrease the serum alanine aminotransferase level and liver index and can alleviate the fat degeneration in liver tissues. Moreover, XKQ can ameliorate insulin resistance and upregulate the expression of IRS-1, PI3K (p85), p-Akt, and GLUT4 in the skeletal muscle of KKAy mice. XKQ is an effective drug for T2DM by ameliorating insulin resistance and regulating the PI3K/Akt signaling pathway in the skeletal muscle.
关键词: XKQ type 2 diabetes mellitus KKAy mice PI3K/Akt pathway diabetic liver disease
RGS16 regulated by let-7c-5p promotes glioma progression by activating PI3K-AKT pathway
《医学前沿(英文)》 2023年 第17卷 第1期 页码 143-155 doi: 10.1007/s11684-022-0929-y
Effects of resistin on insulin signaling in endothelial cells
Zhizhen LI, Fangping LI, Jianhong YE, Li YAN, Zuzhi FU
《医学前沿(英文)》 2009年 第3卷 第2期 页码 136-140 doi: 10.1007/s11684-009-0029-2
关键词: resistin endothelium nitric oxide endothelial nitric oxide synthase Akt-binding protein mouse
Acetyl salicylic acid attenuates cardiac hypertrophy through Wnt signaling
null
《医学前沿(英文)》 2015年 第9卷 第4期 页码 444-456 doi: 10.1007/s11684-015-0421-z
Ventricular hypertrophy is a powerful and independent predictor of cardiovascular morbid events. The vascular properties of low-dose acetyl salicylic acid (aspirin) provide cardiovascular benefits through the irreversible inhibition of platelet cyclooxygenase 1; however, the possible anti-hypertrophic properties and potential mechanism of aspirin have not been investigated in detail. In this study, healthy wild-type male mice were randomly divided into three groups and subjected to transverse aortic constriction (TAC) or sham operation. The TAC-operated mice were treated with the human equivalent of low-dose aspirin (10 mg·kg−1·d−1); the remaining mice received an equal amount of phosphate buffered saline with 0.65% ethanol, which was used as a vehicle. A cardiomyocyte hypertrophy model induced by angiotensin II (10 nmol·L−1) was treated with the human equivalent of low (10 or 100 µmol·L−1) and high (1000 µmol·L−1) aspirin concentrations in plasma. Changes in the cardiac structure and function were assessed through echocardiography and transmission electron microscopy. Gene expression was determined through RT-PCR and western blot analysis. Results indicated that aspirin treatment abrogated the increased thickness of the left ventricular anterior and posterior walls, the swelling of mitochondria, and the increased surface area in in vivo and in vitro hypertrophy models. Aspirin also normalized the upregulated hypertrophic biomarkers, β-myosin heavy chain (β-MHC), atrial natriuretic peptide (ANP), and b-type natriuretic peptide (BNP). Aspirin efficiently reversed the upregulation of β-catenin and P-Akt expression and the TAC- or ANG II-induced downregulation of GSK-3β. Therefore, low-dose aspirin possesses significant anti-hypertrophic properties at clinically relevant concentrations for anti-thrombotic therapy. The downregulation of β-catenin and Akt may be the underlying signaling mechanism of the effects of aspirin.
Effects of phosphatidylinositol 3-kinase inhibitor on human cervical carcinoma cells
Yuan ZHANG MD , Xiaoyan ZHANG MM , Yanhui LI MM , Xuan DU MM , Zehua WANG MD, PhD , Hongbo WANG MD ,
《医学前沿(英文)》 2009年 第3卷 第3期 页码 341-346 doi: 10.1007/s11684-009-0067-9
关键词: human cervical cancer cells apoptosis phosphatidylinositol 3-kinase (PI3K)/Akt FLICE-like inhibitory protein
标题 作者 时间 类型 操作
GDF15 negatively regulates chemosensitivity via TGFBR2-AKT pathway-dependent metabolism in esophageal
期刊论文
Ultraviolet-B induced expression of hypoxia-inducible factor 1α, transferrin receptor through EGFR/PI3K/AKT
LI Yanhua, BI Zhigang
期刊论文
Xiao Ke Qing improves glycometabolism and ameliorates insulin resistance by regulating the PI3K/Akt pathway
Xiaoqing Li, Xinxin Li, Genbei Wang, Yan Xu, Yuanyuan Wang, Ruijia Hao, Xiaohui Ma
期刊论文
Effects of resistin on insulin signaling in endothelial cells
Zhizhen LI, Fangping LI, Jianhong YE, Li YAN, Zuzhi FU
期刊论文