Institution
Xuzhou Medical College
Education•Xuzhou, China•
About: Xuzhou Medical College is a education organization based out in Xuzhou, China. It is known for research contribution in the topics: Cancer & Cell growth. The organization has 12721 authors who have published 7802 publications receiving 102970 citations.
Topics: Cancer, Cell growth, Apoptosis, Medicine, Protein kinase B
Papers published on a yearly basis
Papers
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TL;DR: In this review, novel approaches to nanoscale delivery of chemotherapy are described and recent progress in this field is discussed.
74 citations
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TL;DR: A one-pot approach to prepare hydrophilic MnO NPs via a polyol-like method with poly (ethylene glycol) (PEG) as both a solvent and surfactant is proposed, indicating the potential promising of PEG-MnO Nps as an alternative contrast agent in MRI scanning.
74 citations
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TL;DR: The data suggest BPA inhibits Sertoli cell proliferation due to its anti-androgenic actions, uncovering novel anti- androgenic mechanisms by which BPA antagonizes AR signaling, contributing to Sertolis cell proliferation suppression and male reproductive toxicology.
74 citations
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TL;DR: It is found that luteolin could attenuate cognitive dysfunction in chronic cerebral hypoperfused rats, as assessed using Morris water maze tests, and a potential therapeutic use of lutesin is suggested for cerebral Hypoperfusion associated Cognitive dysfunction in AD.
Abstract: Chronic cerebral hypoperfusion, a mild ischemic condition, is associated with the cognitive deficits of Alzheimer's disease (AD). Luteolin, a polyphenolic compound found in foods of plant origin, belonging to the flavone subclass of flavonoids, has been shown to possess antioxidant, anti-inflammatory and antitumorigenic properties. In the present study, the effects of luteolin on chronic cerebral hypoperfusion-associated neurocognitive pathologies were investigated by using rats with permanent bilateral common carotid artery occlusion, a rat model of chronic cerebral hypoperfusion. As expected, we found that luteolin could attenuate cognitive dysfunction in chronic cerebral hypoperfused rats, as assessed using Morris water maze tests. Daily oral administration of luteolin (50, 100 and 200mg/kg) significantly scavenged oxygen free radicals, enhanced antioxidant potential, decreased the lipid peroxide production and suppressed inflammatory reaction in the cerebral cortex and hippocampus induced by chronic cerebral hypoperfusion. Meanwhile, the results indicated that cerebral hypoperfusion activated nuclear factor-κB (NF-κB), increased the expression of β-site amyloid precursor protein cleaving enzyme (BACE1), as well as elevated amyloid beta (Aβ) levels in the cortex and hippocampus. However, long-term administration of luteolin significantly down-regulated the expression of NF-κB and BACE1, accompanied by diminishing the deposition of Aβ. Our results suggest a potential therapeutic use of luteolin for cerebral hypoperfusion associated cognitive dysfunction in AD.
73 citations
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TL;DR: It is suggested that ROS serves an important role in mediating high glucose-induced EMT and inhibits activation of the TGF-β1/PI3K/Akt/mTOR pathway, and may have potential as a treatment approach to prevent renal fibrosis in DN.
Abstract: Oxidative stress has been reported to serve an important role in the development and progression of diabetic nephropathy (DN). Epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells promotes renal fibrosis in DN, while the mechanism of reactive oxygen species (ROS)-mediated EMT is not fully understood. The aim of the present study was to investigate the effect of high glucose-induced ROS on the activation of the transforming growth factor (TGF)-β1/phosphoinositide 3 kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway in a normal rat kidney tubular epithelial cell line (NRK-52E) and rats with type 1 diabetes. In vitro, high glucose-stimulated ROS production resulted in increased TGF-β1 expression as well as an increase in the Akt and mTOR phosphorylation ratio, resulting in EMT. When cells were pre-treated with ROS inhibitors, changes in TGF-β1, Akt and mTOR were significantly ameliorated. In vivo, diabetic rats experienced a significant decline in renal function and severe renal fibrosis compared with control rats at 8 weeks following streptozocin injection. Levels of malondialdehyde and TGF-β1/PI3K/Akt/mTOR pathway activation were increased in the renal cortex of rats with diabetes compared with the control rats. Furthermore, renal fibrosis was further aggravated in DN compared with the control rats. The results of the present study suggest that ROS serves an important role in mediating high glucose-induced EMT and inhibits activation of the TGF-β1/PI3K/Akt/mTOR pathway. ROS may therefore have potential as a treatment approach to prevent renal fibrosis in DN.
73 citations
Authors
Showing all 12775 results
Name | H-index | Papers | Citations |
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Liang Wang | 98 | 1718 | 45600 |
Chang Liu | 97 | 1099 | 39573 |
Wei Wang | 95 | 3544 | 59660 |
Yu Liu | 66 | 1262 | 20577 |
Deling Kong | 65 | 388 | 16515 |
Zhimou Yang | 61 | 222 | 12522 |
Xu-Feng Huang | 61 | 332 | 13074 |
Guangming Lu | 60 | 476 | 13218 |
Dan Ding | 59 | 212 | 12494 |
Jian Cao | 58 | 486 | 11074 |
Yuanjin Zhao | 57 | 328 | 12076 |
Jie Yang | 56 | 488 | 11382 |
Lei Wang | 54 | 1076 | 15189 |
Xiaodong Shi | 52 | 323 | 8910 |
Wei Pan | 50 | 408 | 9037 |