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Your search keyword '"Zhang, Tian"' showing total 13 results
Start Over Author "Zhang, Tian" Search Limiters Peer Reviewed Publication Year Range Last 50 years Journal biomed research international
13 results on '"Zhang, Tian"'

9. Stem Cell Therapy for Lower Extremity Diabetic Ulcers: Where Do We Stand?

Author

Yang, Mei, Sheng, Lingling, Zhang, Tian R., and Li, Qingfeng

Subjects
Article Subject
Abstract

The impairment of wound healing in diabetic patients is an important clinical problem affecting millions of patients worldwide. Various clinical and basic science studies show that stem cell therapy, as a regenerative medical therapy, can be a good solution. In this paper, we begin with an introduction of the cellular mechanism of the diabetic ulcer. We will then discuss the advantages and limitations of various stem cell therapies that have been under extensive recent study.

Published
2013
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12. Simultaneous Identification and Quantification of Canrenone and 11-α-Hydroxy-Canrenone by LC-MS and HPLC-UVD

Author

Huang, Da-Ming, Zhang, Tian-Zhen, Cui, Feng-Jie, Sun, Wen-Jing, Zhao, Li-Ming, Yang, Meng-Yi, and Wang, Ya-Juan

Abstract

A procedure for simultaneous identification and quantification of canrenone and its biotransformed product 11-α-hydroxy-canrenone by high-performance liquid chromatography with ultraviolet detector (HPLC-UVD) and mass spectrometry (LC-MS) methods was proposed. The optimal determination variables on the HPLC-UVD or LC-MS coupled with a ZORBAX Eclipse XDB-C18 column (150 mm × 4.6 mm, 5 μm) were set as follows: detection wavelength of 280 nm, mobile phase of water and methanol gradient elution, temperature for the chromatographic column of 30°C, flow rate of mobile phase of 0.8 mL/min, sample injection volume of 5 μL, and elution time of 40 min. The MS conditions were set as follows: the flow rate of sheath gas, aux gas, and sweep gas were kept at 35 arb, 5 arb, and 0 arb, respectively. The temperature of capillary was held at 300°C, and capillary voltage was set at 30.00 V. Tube lens were performed at 100.00 V. The proposed method was validated by linearity (𝑟2 ≥ 0.9910), average recovery (94.93%, RSD1.21%), precision (RSD ≤ 1.31%), limit of detection, and limit of quantification (LOD 0.1~0.12 mg/L, LOQ 0.5~0.67 mg/L), which proved to be affordable for simultaneously determining canrenone and its bio-transformed product 11-α-hydroxy-canrenone.

Published
2011
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13. Pinocembrin protects human brain microvascular endothelial cells against fibrillar amyloid-β(1-40) injury by suppressing the MAPK/NF-κB inflammatory pathways.

Author

Liu R, Li JZ, Song JK, Sun JL, Li YJ, Zhou SB, Zhang TT, and Du GH

Subjects
Brain drug effects, Brain pathology, Cell Death drug effects, Cytokines metabolism, Cytoprotection drug effects, Endothelial Cells drug effects, Endothelial Cells metabolism, Flavanones chemistry, Humans, Inflammation Mediators metabolism, Microvessels drug effects, Microvessels pathology, Neuroprotective Agents chemistry, Neuroprotective Agents pharmacology, Oxidation-Reduction drug effects, Signal Transduction drug effects, Amyloid beta-Peptides toxicity, Brain blood supply, Endothelial Cells pathology, Flavanones pharmacology, Inflammation pathology, Mitogen-Activated Protein Kinases metabolism, NF-kappa B metabolism
Abstract

Cerebrovascular accumulation of amyloid-β (Aβ) peptides in Alzheimer's disease (AD) may contribute to disease progression through Aβ-induced microvascular endothelial pathogenesis. Pinocembrin has been shown to have therapeutic effects in AD models. These effects correlate with preservation of microvascular function, but the effect on endothelial cells under Aβ-damaged conditions is unclear. The present study focuses on the in vitro protective effect of pinocembrin on fibrillar Aβ(1-40) (fAβ(1-40)) injured human brain microvascular endothelial cells (hBMECs) and explores potential mechanisms. The results demonstrate that fAβ(1-40)-induced cytotoxicity in hBMECs can be rescued by pinocembrin treatment. Pinocembrin increases cell viability, reduces the release of LDH, and relieves nuclear condensation. The mechanisms of this reversal from Aβ may be associated with the inhibition of inflammatory response, involving inhibition of MAPK activation, downregulation of phosphor-IKK level, relief of IκBα degradation, blockage of NF-κB p65 nuclear translocation, and reduction of the release of proinflammatory cytokines. Pinocembrin does not show obvious effects on regulating the redox imbalance after exposure to fAβ(1-40). Together, the suppression of MAPK and the NF-κB signaling pathways play a significant role in the anti-inflammation of pinocembrin in hBMECs subjected to fAβ(1-40). This may serve as a therapeutic agent for BMEC protection in Alzheimer's-related deficits.

Published
2014
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