Cytotoxic effects of Avermectin on human HepG2 cells in vitro bioassays

Zhang, Yang; Wu, Jigang; Xu, Wenping; Gao, Jufang; Hong-ping, Cao; Yang, Mingjun; Wang, Bo; Hao, Youwu; Tao, Liming

doi:10.1016/j.envpol.2016.11.022

Cited by 48 publications

(23 citation statements)

References 28 publications

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“…Moreover, ABA can induce apoptosis in King pigeon brain neurons and pigeon liver and inhibit the goat liver carbonic anhydrase enzyme . In vitro bioassays, ABA induces HeLa and HepG2 cell DNA damage and apoptosis …”

Section: Discussionmentioning

confidence: 73%

Abamectin induces apoptosis and autophagy by inhibiting reactive oxygen species‐mediated PI3K/AKT signaling in MGC803 cells

Zhu

Zhou

et al. 2019

J Biochem & Molecular Tox

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Abamectin (ABA) is one of the most widely used compounds in agriculture and veterinary medicine. However, the cytotoxicity of ABA in human gastric cells is utterly unknown. In this study, ABA suppressed the proliferation of MGC803 cells by arresting the cell cycle at the G0/G1-phase. Moreover, ABA induced mitochondrialmediated apoptosis by inducing the loss of mitochondrial membrane potential, upregulation of Bax/Bcl-2, and activation of caspase-3. ABA significantly improved the LC3-II/LC3-I ratio and reduced P62 protein expression in a dose-dependent manner. Through detection of the reactive oxygen species (ROS) levels, we found ABA induced the accumulation of intracellular ROS and then reduced PI3K/AKT signaling activation related to MGC803 cell apoptosis and autophagy. Our results indicate that ABA exerts cytotoxic effects on human MGC803 cells through apoptosis and autophagy by inhibiting ROS-mediated PI3K/AKT signaling. Furthermore, ABA may be a potential risk to human gastric health. K E Y W O R D S abamectin, AKT, apoptosis, autophagy, PI3K, reactive oxygen species

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Section: Discussionmentioning

confidence: 73%

Abamectin induces apoptosis and autophagy by inhibiting reactive oxygen species‐mediated PI3K/AKT signaling in MGC803 cells

Zhu

Zhou

et al. 2019

J Biochem & Molecular Tox

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“…It is well known that three pathways can lead to cell death, namely apoptosis, autophagy and cell necrosis . At present, targeting apoptosis is the most successful way to treat cancer in addition to surgery.…”

Section: Discussionmentioning

confidence: 99%

Ivermectin induces cell cycle arrest and apoptosis of HeLa cells via mitochondrial pathway

et al. 2018

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Objectives The aim of study was to investigate the anticancer activities of Ivermectin (IVM) and the possible mechanisms in cells level via cell proliferation inhibition, apoptosis and migration inhibition in model cancer cell HeLa. Materials and methods The MTT assay was used to study the inhibitory effect of IVM on the proliferation of Hela cells, and the cell cycle was analysed by flow cytometry. The neutral comet assay was used to study the DNA damage. The presence of apoptosis was confirmed by DAPI nuclear staining and flow cytometry. Changes in mitochondrial membrane potential and reactive oxygen species (ROS) levels were determined using Rhodamine 123 staining and DCFH‐DA staining. Western blot analysis for apoptosis‐related proteins was carried out. We use scratch test to analyse the antimigration potential of IVM . Results Ivermectin can inhibit the viability of HeLa cells significantly. In addition, treatment with IVM resulted in cell cycle arrest at the G1/S phase which partly account for the suppressed proliferation. Typical apoptosis morphological changes were shown in IVM treatment cells including DNA fragmentation and chromatin condensation. At the same time, the results of flow cytometry analysis showed that the number of apoptotic cells increased significantly with the increase of IVM concentration. Moreover, we observed that the mitochondrial membrane potential collapses and the ratio of Bax/Bcl‐2 in the cytoplasm increases, which induces cytochrome c release from the mitochondria to the cytoplasm, activates caspase‐9/‐3 and finally induces apoptosis. We also found that IVM can significantly increase intracellular ROS content. At the same time, we determined that IVM can significantly inhibit the migration of HeLa cells. Conclusions Our experimental results show that IVM might be a new potential anticancer drug for therapy of human cancer.

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“…The three pathways leading to cell death are autophagy, apoptosis, and necrosis [47]. Most current anticancer drugs induce apoptosis of cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Coix lacryma-jobi var. ma-yuen Stapf sprout extract induces cell cycle arrest and apoptosis in human cervical carcinoma cells

Son¹,

Kim²,

Kim³

et al. 2019

BMC Complement Altern Med

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BackgroundCervical cancer is the second-leading cause of cancer-related mortality in females. Coix lacryma-jobi L. var. ma-yuen (Rom.Caill.) Stapf ex Hook. f. is the most widely recognized medicinal herb for its remedial effects against inflammation, endocrine system dysfunctions, warts, chapped skin, rheumatism, and neuralgia and is also a nourishing food.MethodsTo investigate the activity of Coix lacryma-jobi sprout extract (CLSE) on cell proliferation in human cervical cancer HeLa cells, we conducted a Cell Counting Kit-8 (CCK-8) assay. Flow-cytometric analysis and western blot analysis were performed to verify the effect of CLSE on the regulation of the cell cycle and apoptosis in HeLa cells.ResultsWe observed that CLSE significantly inhibited cell proliferation. Furthermore, CLSE dose-dependently promoted cell cycle arrest at the sub-G1/ S phase in HeLa cells, as detected by bromodeoxyuridine (BrdU) staining. The cell-cycle-arrest effects of CLSE in HeLa cells were associated with downregulation of cyclin D1 and cyclin-dependent kinases (CDKs) 2, 4, and 6. Moreover, CLSE induced apoptosis, as determined by flow-cytometric analysis and nuclear DNA fragmentation with Annexin V/propidium iodide (PI) and 4′6′-diamidino-2-phenylindole (DAPI) staining. Induction of apoptosis by CLSE was involved in inhibition of the antiapoptotic protein B-cell lymphoma 2 (Bcl-2) and upregulation of the apoptotic proteins p53, cleaved poly (ADP-ribose) polymerase (PARP), cleaved caspase-3, and cleaved caspase-8. Finally, we observed that CLSE inactivated the phosphoinositide 3-kinase (PI3K) and protein kinase B (AKT) pathways.ConclusionsCLSE causes cell cycle arrest and apoptotic cell death through inactivation of the PI3K/AKT pathway in HeLa cells, suggesting it is a viable therapeutic agent for cervical cancer owing to its anticancer effects.

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Cytotoxic effects of Avermectin on human HepG2 cells in vitro bioassays

Cited by 48 publications

References 28 publications

Abamectin induces apoptosis and autophagy by inhibiting reactive oxygen species‐mediated PI3K/AKT signaling in MGC803 cells

Abamectin induces apoptosis and autophagy by inhibiting reactive oxygen species‐mediated PI3K/AKT signaling in MGC803 cells

Ivermectin induces cell cycle arrest and apoptosis of HeLa cells via mitochondrial pathway

Coix lacryma-jobi var. ma-yuen Stapf sprout extract induces cell cycle arrest and apoptosis in human cervical carcinoma cells

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