Inductive effect of hydroxyl safflower yellow-A on apoptosis in abnormal HUVEC via the mitochondrial pathway

Si, Na; Wang, Jingjing; Xu, Yingying; Liu, Lintao; Wang, Xu; Sun, Haixiang; Lin, Zong; Wang, Xixi; Liu, Li; Zhang, Qi; Zhang, Qian; Feng, Cuiping

doi:10.1016/j.jtcms.2015.05.001

Cited by 3 publications

(5 citation statements)

References 13 publications

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“…HSYA is one of the primary water-soluble, active ingredients of the TCM safflower. HSYA has been reported to promote apoptosis in abnormal human umbilical vein endothelial cells (29) and to suppress the inflammatory responses of BV2 microglial cells after oxygen-glucose deprivation (30). In the present study, an MTT assay revealed that HSYA reduced the viability of liver cancer cells and a large number of vacuoles and a small amount of cell debris were microscopically observed in HSYA-treated cells, suggesting that HSYA induced autophagy.…”

Section: Discussionsupporting

confidence: 55%

Hydroxysafflor yellow�A induces autophagy in human liver cancer cells by regulating Beclin�1 and ERK expression

Chen

Liu

et al. 2020

Exp Ther Med

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Hydroxysafflor yellow A (HSYA) is a water-soluble component of the safflower (Carthamus tinctorius), and research has revealed that HSYA exhibits antitumor effects. In the present study, the effects of HSYA on the autophagy of a Hep-G2 liver cancer cell line, as well as the underlying mechanisms, were investigated. Hep-G2 cells were treated with HSYA and the viability of cells was measured using an MTT assay. Western blotting and immunofluorescence assays were performed to determine the expression of light chain 3 II (LC3-II) and p62, as well as the autophagy regulators Beclin 1 and ERK1/2. Transmission electron microscopy was performed to observe the formation of autophagosomes. The combined effects of HSYA and the autophagy inhibitor chloroquine (CQ) were also determined. The results revealed that the viability of Hep-G2 cells decreased with increasing concentrations of HSYA. Furthermore, LC3-II expression increased significantly and the level of p62 decreased significantly in the HYSA group compared with the control group. Additionally, an increase in Beclin 1 expression and a decrease in phosphorylated-ERK1/2 expression was observed in Hep-G2 cells treated with HYSA. Following treatment with CQ and HSYA, a significant increase in the viability of Hep-G2 cells was observed compared with the HSYA group. Collectively, the results indicated that HSYA induced autophagy by promoting the expression of Beclin 1 and inhibiting the phosphorylation of ERK in liver cancer cells. Therefore, HSYA may serve as a potential therapeutic agent for liver cancer.

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Section: Discussionsupporting

confidence: 55%

Hydroxysafflor yellow�A induces autophagy in human liver cancer cells by regulating Beclin�1 and ERK expression

Chen

Liu

et al. 2020

Exp Ther Med

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“…Studies have reported that natural anti-cancer agents have powerful effects in controlling cancers [ 24 – 26 ]. Our group has focussed on anti-tumor research of HSYA for almost a decade, and we found that HSYA suppresses tumor growth by inhibiting cell proliferation [ 12 , 13 ] and angiogenesis [ 4 , 13 , 14 , 27 ], and inducing cell apoptosis. In the present study, MTT assay showed that HSYA and PPAR-γ agonist RGZ significantlyinhibited BGC-823 cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

“…The mechanism of apoptosis by HSYA may be related to activation of the mitochondrial apoptotic pathway and regulation of expressions of Bcl-2, Bax, and p53 [ 12 ]. Caspase family members play a critical role in the apoptotic pathway, and are mainly involved in a series of caspase activations, which are regulated to the extrinsic pathway and the intrinsic pathway.…”

Section: Discussionmentioning

confidence: 99%

“…HSYA was also reported to suppress tumor growth by inhibiting cell proliferation [ 12 , 13 ] and angiogenesis [ 8 , 14 ], and inducing cell apoptosis [ 9 , 15 ]. Since many signal factors (e.g., Bcl-2, Bax, and caspase-3) in numerous apoptotic pathways can be mediated by HSYA [ 9 , 12 , 13 ], it may function as a common molecular target to activate various downstream apoptotic signals and promote tumor cell apoptosis. Moreover, peroxisome proliferator-activated receptorγ (PPARγ) is also associated with these signal factors [ 16 – 18 ].…”

Section: Introductionmentioning

confidence: 99%

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Hydroxysafflor-Yellow A Induces Human Gastric Carcinoma BGC-823 Cell Apoptosis by Activating Peroxisome Proliferator-Activated Receptor Gamma (PPARγ)

Liu

et al. 2018

Med Sci Monit

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BackgroundAnti-tumor properties of hydroxysafflor-yellow A (HSYA) have been recently revealed, as a series of apoptotic factors were confirmed to be regulated by HSYA and associated with peroxisome proliferator-activated receptor Gamma (PPARγ). In this study, we investigated the cell apoptosis mechanism of HSYA via activated PPARγ signal in human gastric carcinoma cells.Material/MethodsBGC-823 cells were cultured and divided into 5 independent groups: Tumor, HSYA, HSYA+PPARγ inhibitor (GW9662), and PPARγ agonist (RGZ), RGZ+GW9662. Cell proliferative activity was measured by MTT. Apoptosis and cell cycle were detected by flow cytometry. The nuclear translocation of PPARγ was detected by immunofluorescence staining chemistry, and mRNA levels of PPARγ and caspase-3 were measured by real-time qPCR.ResultsCompared to the RGZ group, the HSYA group (100 μM) showed a similar inhibitory effect on the proliferation process of BGC-823 cells, inducing their apoptosis. As a result, the transition of BGC-823 cells from G0/G1 phase to S phase was blocked. HSYA was also found to promote the nuclear translocation of PPARγ, leading to increased expression of PPARγ and caspase-3. The regulatory effect of HSYA on BGC-823 cells could be further inhibited by PPARγ inhibitor in group GW9662.ConclusionsWe report the inhibitory effect of HSYA on the proliferation of BGC-823 cells, which results in activating PPARγ-dependent cell cycle blocking and cell apoptosis, suggesting that PPARγ is a specific type of HSYA that can induce apoptosis of BGC-823 cells.

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“…Analogous findings revealed that protein expression of Bax was also increased, while those of Bcl-2, Fas and Fas-L (Fas ligand) were decreased. The mechanism of hydroxy safflower yellow A-induced apoptosis of HUVECs stimulated by the supernatant of tumor cells activation was attributed to the mitochondrial apoptotic pathway and regulation of the expressions of apoptosis-controlling proteins [ 165 ]. The effect of hydroxy safflower yellow A on vasculogenesis and its molecular mechanism was determined by investigating the expression of ERK/MAPK and NF-κB signaling pathway in H22 (hepatoma) tumor-bearing mice.…”

Section: Effect Of Polyphenols On Angiogenesismentioning

confidence: 99%

Antiangiogenic Effect of Flavonoids and Chalcones: An Update

Mirossay

Varinská

Mojžiš

2017

IJMS

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Chalcones are precursors of flavonoid biosynthesis in plants. Both flavonoids and chalcones are intensively investigated because of a large spectrum of their biological activities. Among others, anticancer and antiangiogenic effects account for the research interest of these substances. Because of an essential role in cancer growth and metastasis, angiogenesis is considered to be a promising target for cancer treatment. Currently used antiangiogenic agents are either synthetic compounds or monoclonal antibodies. However, there are some limitations of their use including toxicity and high price, making the search for new antiangiogenic compounds very attractive. Nowadays it is well known that several natural compounds may modulate basic steps in angiogenesis. A lot of studies, also from our lab, showed that phytochemicals, including polyphenols, are potent modulators of angiogenesis. This review paper is focused on the antiangiogenic effect of flavonoids and chalcones and discusses possible underlying cellular and molecular mechanisms.

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Inductive effect of hydroxyl safflower yellow-A on apoptosis in abnormal HUVEC via the mitochondrial pathway

Cited by 3 publications

References 13 publications

Hydroxysafflor yellow�A induces autophagy in human liver cancer cells by regulating Beclin�1 and ERK expression

Hydroxysafflor yellow�A induces autophagy in human liver cancer cells by regulating Beclin�1 and ERK expression

Hydroxysafflor-Yellow A Induces Human Gastric Carcinoma BGC-823 Cell Apoptosis by Activating Peroxisome Proliferator-Activated Receptor Gamma (PPARγ)

Antiangiogenic Effect of Flavonoids and Chalcones: An Update

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