ArticleScientific reports2015
E. adenophorum induces Cell Cycle Arrest and Apoptosis of Splenocytes through the Mitochondrial Pathway and Caspase Activation in Saanen Goats.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 25 citations in OpenAlex.
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- Arbuscular mycorrhizal fungi improve the competitive advantage of a native plant relative to a congeneric invasive plant in growth and nutrition.Ecology and evolution · 2024Article
- Ageratina adenophora damages the rumen epithelium via inducing the expression of inflammatory factors in goats.Journal of animal science · 2024Article
- Piceatannol improved cerebral blood flow and attenuated JNK3 and mitochondrial apoptotic pathway in a global ischemic model to produce neuroprotection.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
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- Ageratina adenophora induces mice hepatotoxicity via ROS-NLRP3-mediated pyroptosis.Scientific reports · 2018Article
- Euptox A Induces G1 Arrest and Autophagy via p38 MAPK- and PI3K/Akt/mTOR-Mediated Pathways in Mouse Splenocytes.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2017Article
- Development of a Functional Glomerulus at the Organ Level on a Chip to Mimic Hypertensive Nephropathy.Scientific reports · 2016Article
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- Involvement of mitochondrial dysfunction in hepatotoxicity induced by Ageratina adenophora in mice.Journal of Zhejiang University. Science. BArticle
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Authors and funding
13 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The precise cytotoxicity of E. Adenophorum in relation to the cell cycle and apoptosis of splenocytes in Saanen goats remains unclear. In the present study, 16 Saanen goats were randomly divided into four groups, which were fed on 0%, 40%, 60% and 80% E. adenophorum diets. The results of TUNEL, DAPI and AO/EB staining, flow cytometry analysis and DNA fragmentation assays showed that E. adenophorum induced typical apoptotic features in splenocytes, suppressed splenocyte viability, and caused cell cycle arrest in a dose-dependent manner. However, westernblot, ELISA, qRT-PCR and caspase activity analyses showed that E. adenophoruminhibited Bcl-2 expression, promoted Bax translocation to the mitochondria, triggered the release of Cytc from the mitochondria into the cytosol, and activated caspase-9 and -3 and the subsequent cleavage of PARP. Moreover, in E. adenophorum-induced apoptosis, the protein levels of Fas, Bid, FasL and caspase-8 showed no significant changes. E. adenophorum treatment induced the collapse of ΔΨm. Moreover, these data suggested that E. adenophorum induces splenocyte apoptosis via the activation of the mitochondrial apoptosis pathway in splenocytes. These findings provide new insights into the mechanisms underlying the effects of E. adenophorum cytotoxicity on splenocytes.
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