E. adenophorum Induces Cell Cycle and Apoptosis of Renal Cells through Mitochondrial Pathway and Caspase Activation in Saanen Goat

He, Ying; Chen, Weihong; Hu, Yanchun; Luo, Biao; Wu, Lei; Qiao, Yan; Mo, Quan; Xu, Ruiguang; Zhou, Yuanjie; Ren, Zhihua; Zuo, Zhicai; Deng, Junliang; Peng, Guangneng; He, Wei; Wei, Yahui

doi:10.1371/journal.pone.0138504

Cited by 18 publications

(16 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies showed that the ingestion of A. adenophora as a feed additive induced hepatotoxicity in mice 28 and rat 7 , as well as chronic pulmonary disease in horses 29 . In our previous studies, apoptosis pathway was triggered by A. adenophora in goat and mice 10 , 30 , 31 . In this study, IL-1β, a pro-inflammatory cytokine, was induced by A. adenophora (Fig.…”

Section: Discussionmentioning

confidence: 92%

Ageratina adenophora induces mice hepatotoxicity via ROS-NLRP3-mediated pyroptosis

Sun

Zeng

Liu

et al. 2018

Sci Rep

Self Cite

View full text Add to dashboard Cite

Increasing evidences have demonstrated that Ageratina adenophora (A. adenophora) can cause hepatotoxicity of animals. Liver is an important site in immune regulation and inflammatory responses. However, the information about hepatotoxicity induced by A. adenophora in relation to inflammation is still finite. To investigate the underlying mechanism, we conducted animal experiments with different dosage of A. adenophora. Mice were randomly divided into 4 groups and administrated with 0%, 10%, 20% and 30% levels of A. adenophora pallet diet in control, group A, B and C, respectively. The results showed that A. adenophora caused hepatotoxicity as revealed by increasing alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase. Then, the reactive oxygen species (ROS) levels were shown to be elicited by A. adenophora through flow cytometry assay in a dose-dependent manner. Furthermore, pyroptosis was activated by A. adenophora, which was characterized by increasing protein and mRNA levels of caspase-1, gasdermin D and interleukin-1β. Notably, ROS down-stream factors, including nod-like receptor inflammasome protein 3 and nuclear factor-κB, were also activated by A. adenophora. These data demonstrated that A. adenophora caused liver inflammatory injury and induced hepatocyte pyroptosis by activating NLRP3 inflammasome, which was triggered by elevating ROS production levels. This research might provide new insights into the mechanism of hepatotoxicity induced by A. adenophora.

show abstract

Section: Discussionmentioning

confidence: 92%

Ageratina adenophora induces mice hepatotoxicity via ROS-NLRP3-mediated pyroptosis

Sun

Zeng

Liu

et al. 2018

Sci Rep

Self Cite

View full text Add to dashboard Cite

show abstract

“…p53 also advances apoptosis through the mitochondrial pathways ( 30 ). The p53-dependent apoptosis leads to mitochondrial apoptotic changes via activation of the Bax and caspases cascade ( 31 ). Furthermore, p53 activates the p21 protein to instigate a the G1 phase cell cycle arrest ( 32 ).…”

Section: Resultsmentioning

confidence: 99%

Extracts of Opuntia humifusa Fruits Inhibit the Growth of AGS Human Gastric Adenocarcinoma Cells

Hahm

Park

et al. 2016

JFN

View full text Add to dashboard Cite

Opuntia humifusa (OHF) has been used as a nutraceutical source for the prevention of chronic diseases. In the present study, the inhibitory effects of ethyl acetate extracts of OHF on the proliferation of AGS human gastric cancer cells and the mode of action were investigated. To elucidate the antiproliferative mechanisms of OHF in cancer cells, the expression of genes related to apoptosis and cell cycle arrest were determined with real-time PCR and western blot. The cytotoxic effect of OHF on AGS cells was observed in a dose-dependent manner. Exposure to OHF (100 μg/mL) significantly induced (P<0.05) the G1 phase cell cycle arrest. Additionally, the apoptotic cell population was greater (P<0.05) in OHF (200 μg/mL) treated AGS cells when compared to the control. The expression of genes associated with cell cycle progression (Cdk4, Cdk2, and cyclin E) was significantly downregulated (P<0.05) by the OHF treatment. Moreover, the expression of Bax and caspase-3 in OHF treated cells was higher (P<0.05) than in the control. These findings suggest that OHF induces the G1 phase cell cycle arrest and activation of mitochondria-mediated apoptosis pathway in AGS human gastric cancer cells.

show abstract

“…Cellular morphological changes were subsequently examined using fluorescence microscopy; live cells were stained green, apoptotic cells, yellow and necrotic cells, red. The percentage of apoptotic cells was calculated using the following formula: Apoptotic rate (%)=(number of apoptotic cells/total number of cells)x100, as previously described (17,18).…”

Section: A549 Cell Culturementioning

confidence: 99%

Knockdown of GluA2 induces apoptosis in non-small-cell lung cancer A549 cells through the p53 signaling pathway

Zhang

Yang

2017

Oncology Letters

View full text Add to dashboard Cite

Abstract. α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors are important glutamatergic receptors that mediate fast excitatory synaptic transmission in the brain. Previous studies have demonstrated that glutamate ionotropic receptor AMPA type subunit 2 (GluA2), one of the four subunits that comprise AMPA receptors, is a potential novel marker for poor prognosis in patients with human lung cancer. However, the mechanisms of GluA2-induced apoptosis, proliferation and migration in lung cancer remain unknown. The present study aimed to explore the mechanisms underlying these effects of GluA2 in human lung cancer by silencing GluA2 in A549 cells. Using the Cell Counting Kit-8 assay, western blot analysis and acridine orange/ethidium bromide staining, downregulation of GluA2 was revealed to significantly inhibit the proliferation and significantly promote the apoptosis of A549 cells. Knockdown of GluA2 was also revealed to be associated with increased caspase-3 activity, increased Bcl-2-associated X protein and Bcl-2-associated death promoter (Bad) expression, and decreased expression of B-cell lymphoma-2, p-Bad and X-linked inhibitor of apoptosis protein. In addition, GluA2 silencing upregulated cellular tumor antigen p53 (p53)/p21Cip1/Waf1 /p16 INK4a protein.In conclusion, these results indicate that the effects of GluA2 in lung cancer are mediated by the caspase-3 and p53/p21Cip1/Waf1 /p16 INK4a signaling pathways. Therefore, GluA2 may be a potential novel therapeutic target for the treatment of lung cancer.

show abstract

E. adenophorum Induces Cell Cycle and Apoptosis of Renal Cells through Mitochondrial Pathway and Caspase Activation in Saanen Goat

Cited by 18 publications

References 42 publications

Ageratina adenophora induces mice hepatotoxicity via ROS-NLRP3-mediated pyroptosis

Ageratina adenophora induces mice hepatotoxicity via ROS-NLRP3-mediated pyroptosis

Extracts of Opuntia humifusa Fruits Inhibit the Growth of AGS Human Gastric Adenocarcinoma Cells

Knockdown of GluA2 induces apoptosis in non-small-cell lung cancer A549 cells through the p53 signaling pathway

Contact Info

Product

Resources

About