Shasha Bai
Guangzhou University of Chinese Medicine
12 Papers
1 Citations
Shasha Bai is an academic researcher from Guangzhou University of Chinese Medicine. The author has contributed to research in topics: Sinomenine & Chemistry. The author has an hindex of 5, co-authored 10 publications.
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Papers
Sinomenine regulates CD14/TLR4, JAK2/STAT3 pathway and calcium signal via α7nAChR to inhibit inflammation in LPS-stimulated macrophages.
Rui-li Zhu,Yingkun Zhi,Lang Yi,Jin-Fang Luo,Jing Li,Shasha Bai,Liang Liu,Pei-xun Wang,Hua Zhou,Hua Zhou,Yan Dong +10 more
TL;DR: SIN can decrease the expression of CD14/TLR4 and intracellular free calcium level, activate JAK2/STAT3 pathway to inhibit inflammatory response through α7nAChR in macrophages.
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Sinomenine inhibits fibroblast-like synoviocyte proliferation by regulating α7nAChR expression via ERK/Egr-1 pathway.
Lang Yi,Yan-jun Lyn,Chong Peng,Rui-li Zhu,Shasha Bai,Liang Liu,Pei-xun Wang,Hua Zhou,Hua Zhou,Yan Dong +9 more
TL;DR: The expression of &agr;7nAChR involved in the aggressive proliferation of FLS induced by TNF‐&agR; and was regulated by ERK/Egr‐1 signal pathway.
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Isoorientin Inhibits Inflammation in Macrophages and Endotoxemia Mice by Regulating Glycogen Synthase Kinase 3β.
Yingui Li,Yijing Zhao,Xiaoqin Tan,Xiaoqin Tan,Jiayan Liu,Yingkun Zhi,Lang Yi,Shasha Bai,Qun Du,Qing X. Li,Yan Dong +10 more
TL;DR: Isoorientin can inhibit GSK3β by increasing p-GSK3β and regulate the downstream signal molecules to inhibit inflammation and protect the integrity of the blood-brain barrier and the homeostasis in the brain.
Inhibitory effect of sinomenine on lung cancer cells via negative regulation of α7 nicotinic acetylcholine receptor
Shasha Bai,Wenhao Wen,Xuenan Hou,Jiexiu Wu,Lang Yi,Yingkun Zhi,Yanjun Lv,Xiaoqin Tan,Liang Liu,Pei-xun Wang,Hua Zhou,Yan Dong +11 more
TL;DR: Sinomenine can inhibit lung cancer via α7 nAChR in a negative feedback mode, and this alkaloid is possibly a natural ligand of this receptor.
23
Arenobufagin Promoted Oxidative Stress-Associated Mitochondrial Pathway Apoptosis in A549 Non-Small-Cell Lung Cancer Cell Line
Jun Kan,Haifu Huang,Zhangyu Jiang,Ruisheng Zhou,Shasha Bai,Caijie Liao,Jiancong Chen,Jun Dong,Yunlong Zhang,Jingzhi Zhang,Rong Zhang,Dai-Han Zhou,En-Xin Zhang +12 more
TL;DR: The data demonstrate that apoptosis in the non-small-cell lung cancer (NSCLC) cell line A549 is caused by oxidative stress due to ARE, and shows that ARE may have the potential to become a targeted therapeutic for the treatment of NSCLC in the future.