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33 results on '"Wang, Yanmao"'

15. Acetylshikonin exerts anti-tumor effects on non-small cell lung cancer through dual inhibition of STAT3 and EGFR

Author

Tang, Yemeng, primary, Wang, Yanmao, additional, Wang, Xian, additional, Zhao, Zhucheng, additional, Cai, Haijian, additional, Xie, Mengyao, additional, Jiang, Xintong, additional, Zhang, Luyao, additional, Cheng, Jiayun, additional, Yang, Lehe, additional, Wang, Liangxing, additional, Zhao, Chengguang, additional, and Huang, Xiaoying, additional

Published
2022
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32. MicroRNA-296-5p promotes healing of diabetic wound by targeting sodium-glucose transporter 2 (SGLT2).

Author

Liu, Xiaomin, Wang, Yanmao, Zhang, Xiaotian, Zhang, Xinju, Guo, Jing, Zhou, Jinbao, Chai, Yimin, Ma, Zhong‐liang, and Ma, Zhong-Liang

Abstract

Background: Diabetic wounds are refractory and very difficult to heal. We aimed to use miRNA to identify novel and specific molecular markers for diabetes mellitus (DM) diagnosis and treatment.Methods: The expression level of miR-296-5p was determined in tissue samples of 12 DM patients. The effect of miR-296-5p on proliferation of β-cells was examined using Cell Counting Kit-8 (CCK-8) and colony formation assay. The effect of miR-296-5p on cell cycle progression was analysed using flow cytometry. The target gene was verified using luciferase reporter assay. A rat diabetes model was used to assess the effect of miR-296-5p in vivo.Results: Overexpression of miR-296-5p suppressed cell proliferation, arrested cell cycle progression, and increased the healing rate of diabetic wounds both in vivo and in vitro. TargetScan analysis results showed that miR-296-5p is a direct regulator of SGLT2.Conclusions: miR-296-5p can increase the healing rate of diabetic wounds and may be an effective molecular tool in DM diagnosis and therapy. [ABSTRACT FROM AUTHOR]

Published
2019
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33. ROS-activated NLRP3 inflammasome initiates inflammation in delayed wound healing in diabetic rats.

Author

Dai J, Zhang X, Wang Y, Chen H, and Chai Y

Abstract

Background: This study aims to evaluate the roles of reactive oxygen species (ROS) generation and inflammasome formation in the development of diabetic rat wound inflammation., Materials and Methods: Diabetes was induced in rats by a single intraperitoneal injection of STZ, and a skin wound (2×2 cm 2 ) was produced on the back. Diabetic animals were treated with NAC and Bay 11-7082 to block ROS and the NLRP3 inflammasome, respectively. Total mRNA and protein were isolated from wound tissue and subjected to real-time polymerase chain reaction, Western blot analyses and ELISA. We also assessed the rate of wound closure and time to wound healing., Results: During healing, the diabetic rat exhibited increased ROS production, NLRP3 inflammasome activation and IL-1β secretion. NAC was responsible for the inhibition of ROS production and NLRP3 inflammasome activation in diabetic rat wounds. We also found that blocking ROS generation improved the impaired healing pattern in diabetic rats and decreased the time for complete skin healing., Conclusion: These data suggest that excessive ROS production contributes to activating NLRP3-IL-1β pathway events and impairs wound healing in a diabetic rat wound model., Competing Interests: None., (IJCEP Copyright © 2017.)

Published
2017

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