Shanshan Wei
Central South University
23 Papers
Shanshan Wei is an academic researcher from Central South University. The author has contributed to research in topics: Medicine & Cardiotoxicity. The author has an hindex of 7, co-authored 13 publications.
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Papers
Network Pharmacology Prediction and Molecular Docking-Based Strategy to Discover the Potential Pharmacological Mechanism of Huai Hua San Against Ulcerative Colitis.
Jiaqin Liu,Jian Liu,Xiao-Liang Tong,Weijun Peng,Shanshan Wei,Taoli Sun,Yi-Kun Wang,Bikui Zhang,Wenqun Li +8 more
TL;DR: In this paper, a network pharmacology-based approach combined with molecular docking and in vitro validation was performed to determine the bioactives, key targets, and potential pharmacological mechanism of Huai Hua San (HHS) against UC.
Anticancer Activity and Mechanism of Xanthohumol: A Prenylated Flavonoid From Hops (Humulus lupulus L.).
TL;DR: This review aims to summarize the existing studies focusing on the anticancer activity of xanthohumol and its effects on key signaling molecules and the limitations of current studies and challenges for the clinical use of Xn.
Xanthohumol, a prenylated flavonoid from Hops, exerts anticancer effects against gastric cancer in vitro
TL;DR: Results suggest that Xn exerts anticancer effects against GC via induction of ROS production and subsequent inhibition of NF-κB signaling, and may be a promising candidate treatment against GC progression.
Nrf2‑dependent antioxidant response mediated the protective effect of tanshinone IIA on doxorubicin‑induced cardiotoxicity
Zhao-hui Guo,Miao Yan,Lei Chen,Ping-Fei Fang,Zhi-hua Li,Zimeng Wan,Si-si Cao,Zhen-yan Hou,Shanshan Wei,Wenqun Li,Bikui Zhang +10 more
TL;DR: Results suggest that the Nrf2-dependent antioxidant response mediates the protective effect of Tan IIA on DOX-induced cardiotoxicity.
Involvement of ROS/NLRP3 Inflammasome Signaling Pathway in Doxorubicin-Induced Cardiotoxicity.
Shanshan Wei,Wanjun Ma,Xiaohui Li,Chuanhao Jiang,Taoli Sun,Yuan-Jian Li,Bikui Zhang,Wenqun Li +7 more
TL;DR: A crucial role of ROS/NLRP3-associated inflammasome activation in Dox-induced cardiotoxicity is revealed, and NLRP3 inflammaome may represent a new therapeutic target for Dox's cardiot toxicity.
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