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Hui Cheng

Researcher at Anhui University

Publications -  5
Citations -  239

Hui Cheng is an academic researcher from Anhui University. The author has contributed to research in topics: Apoptosis & p38 mitogen-activated protein kinases. The author has an hindex of 4, co-authored 5 publications receiving 212 citations.

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Involvement of ubiquitin proteasome system in protective mechanisms of Puerarin to MPP+-elicited apoptosis

TL;DR: Perarin could protect MPP(+)-induced SH-SY5Y cells from apoptosis by regulating the function of UPS, as evidenced by promoting cell viability, improving morphological changes and reducing apoptotic rate.
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Gambogenic acid inhibits proliferation of A549 cells through apoptosis-inducing and cell cycle arresting.

TL;DR: The results suggested that GNA significantly inhibited the proliferation of several tumor cell lines in vitro and in vivo and might suggest that G NA inhibits tumor cell proliferation via apoptosis-induction and cell cycle arrest.
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Gambogenic acid induced mitochondrial-dependent apoptosis and referred to phospho-Erk1/2 and phospho-p38 MAPK in human hepatoma HepG2 cells.

TL;DR: Results indicated that gambogenic acid induced mitochondrial oxidative stress and activated caspases through a caspase-3 and casp enzyme-9-dependent apoptosis pathway and was involved in the phospho-Erk1/2 and phospho -p38 MAPK proteins expression changes in HepG2 cells.
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Gambogenic acid inhibits proliferation of A549 cells through apoptosis inducing through up-regulation of the p38 MAPK cascade.

TL;DR: This paper investigated whether GNA-induced apoptosis is critically mediated by the p38 mitogen-activated protein kinase (MAPK) pathway and suggested that up-regulation of the p 38 MAPK cascade may account for the activation of GNA's induced apoptosis.
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[Gambogenic acid inhibits proliferation of A549 cells through apoptosis-inducing].

TL;DR: The results indicate that GNA could affect the development and progression of A549 cells through inducing apoptosis, mediating the expression of VEGF in vascular cells and COX-2 in tumor cells.