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Saikosaponin d induces cell death through caspase-3-dependent, caspase-3-independent and mitochondrial pathways in mammalian hepatic stellate cells

Overview of attention for article published in BMC Cancer, July 2016
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Title
Saikosaponin d induces cell death through caspase-3-dependent, caspase-3-independent and mitochondrial pathways in mammalian hepatic stellate cells
Published in
BMC Cancer, July 2016
DOI 10.1186/s12885-016-2599-0
Pubmed ID
Authors

Ming-Feng Chen, S. Joseph Huang, Chao-Cheng Huang, Pei-Shan Liu, Kun-I Lin, Ching-Wen Liu, Wen-Chuan Hsieh, Li-Yen Shiu, Chang-Han Chen

Abstract

Saikosaponin d (SSd) is one of the main active triterpene saponins in Bupleurum falcatum. It has a steroid-like structure, and is reported to have pharmacological activities, including liver protection in rat, cell cycle arrest and apoptosis induction in several cancer cell lines. However, the biological functions and molecular mechanisms of mammalian cells under SSd treatment are still unclear. The cytotoxicity and apoptosis of hepatic stellate cells (HSCs) upon SSd treatment were discovered by MTT assay, colony formation assay and flow cytometry. The collage I/III, caspase activity and apoptotic related genes were examined by quantitative PCR, Western blotting, immunofluorescence and ELISA. The mitochondrial functions were monitored by flow cytometry, MitoTracker staining, ATP production and XF24 bioenergetic assay. This study found that SSd triggers cell death via an apoptosis path. An example of this path might be typical apoptotic morphology, increased sub-G1 phase cell population, inhibition of cell proliferation and activation of caspase-3 and caspase-9. However, the apoptotic effects induced by SSd are partially blocked by the caspase-3 inhibitor, Z-DEVD-FMK, suggesting that SSd may trigger both HSC-T6 and LX-2 cell apoptosis through caspase-3-dependent and independent pathways. We also found that SSd can trigger BAX and BAK translocation from the cytosol to the mitochondria, resulting in mitochondrial function inhibition, membrane potential disruption. Finally, SSd also increases the release of apoptotic factors. The overall analytical data indicate that SSd-elicited cell death may occur through caspase-3-dependent, caspase-3-independent and mitochondrial pathways in mammalian HSCs, and thus can delay the formation of liver fibrosis by reducing the level of HSCs.

Mendeley readers

The data shown below were compiled from readership statistics for 21 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
India 1 5%
Unknown 20 95%

Demographic breakdown

Readers by professional status Count As %
Student > Postgraduate 3 14%
Student > Bachelor 3 14%
Researcher 3 14%
Student > Master 3 14%
Student > Ph. D. Student 2 10%
Other 3 14%
Unknown 4 19%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 6 29%
Medicine and Dentistry 3 14%
Agricultural and Biological Sciences 2 10%
Psychology 1 5%
Social Sciences 1 5%
Other 3 14%
Unknown 5 24%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 22 August 2016.
All research outputs
#7,144,879
of 8,261,086 outputs
Outputs from BMC Cancer
#2,811
of 3,475 outputs
Outputs of similar age
#213,711
of 253,387 outputs
Outputs of similar age from BMC Cancer
#162
of 233 outputs
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So far Altmetric has tracked 3,475 research outputs from this source. They receive a mean Attention Score of 3.6. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 253,387 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 233 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.