The apoptotic and autophagic properties of two natural occurring prodrugs, hyperoside and hypoxoside, against pancreatic cancer cell lines

Boukes, Gerhardt J.; Venter, Maryna van de

doi:10.1016/j.biopha.2016.07.029

Cited by 28 publications

(27 citation statements)

References 32 publications

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“…The biofunctions of hyperoside were mainly involved in antioxidants, hypoglycemic, anti-cancer, anti-inflammatory and cardiovascular effects [19]. Previous studies have showed that hyperoside can help with the amelioration of lung cancer [20], pancreatic cancer [21], prostate cancer [22] and colon cancer [23]. However, whether hyperoside has therapeutic effects on breast cancer remains elusive.…”

Section: Introductionmentioning

confidence: 99%

Hyperoside Induces Breast Cancer Cells Apoptosis via ROS-Mediated NF-κB Signaling Pathway

Qiu

Zhang

Zhu

et al. 2019

IJMS

111

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Hyperoside (quercetin 3-o-β-d-galactopyranoside) is one of the flavonoid glycosides with anti-inflammatory, antidepressant, and anti-cancer effects. But it remains unknown whether it had effects on breast cancer. Here, different concentrations of hyperoside were used to explore its therapeutic potential in both breast cancer cells and subcutaneous homotransplant mouse model. CCK-8 and wound healing assays showed that the viability and migration capability of Michigan Cancer Foundation-7 (MCF-7) and 4T1 cells were inhibited by hyperoside, while the apoptosis of cells were increased. Real-time quantitative PCR (qRT-PCR) and western blot analysis were used to detect mRNA and the protein level, respectively, which showed decreased levels of B cell lymphoma-2 (Bcl-2) and X-linked inhibitor of apoptosis (XIAP), and increased levels of Bax and cleaved caspase-3. After exploration of the potential mechanism, we found that reactive oxygen species (ROS) production was reduced by the administration of hyperoside, which subsequently inhibited the activation of NF-κB signaling pathway. Tumor volume was significantly decreased in subcutaneous homotransplant mouse model in hyperoside-treated group, which was consistent with our study in vitro. These results indicated that hyperoside acted as an anticancer drug through ROS-related apoptosis and its mechanism included activation of the Bax–caspase-3 axis and the inhibition of the NF-κB signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Hyperoside Induces Breast Cancer Cells Apoptosis via ROS-Mediated NF-κB Signaling Pathway

Qiu

Zhang

Zhu

et al. 2019

IJMS

111

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“…Hyperin, a flavonoid compound occurring in natural plants, has been demonstrated to exert a variety of biological activities, including antioxidant 11,12 , anti-inflammatory 13 , anticancer 14 , and cardiovascular protective effects 15 . Besides, hyperin is reported to have hepato-protective activity 16,17 .…”

Section: ■ Introductionmentioning

confidence: 99%

Hyperin protects against cisplatin-induced liver injury in mice

Niu

Han

et al. 2017

Acta Cir. Bras.

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Purpose: To evaluate the effect of hyperin in cisplatin-induced liver injury in mice. Methods: Mice were pretreated with hyperin at doses of 25 mg/kg and 50 mg/kg, respectively, for six days, and intraperitoneal injection of cisplatin (40 mg/kg) was administrated one hour after the final intragastrication of hyperin. Twenty-four hours later, blood and liver were collected for further research. Results: A single injection of cisplatin (40 mg/kg) for 24 h significantly increased serum alanine and aspartate aminotransferases (ALT/AST) and gamma glutamyl transferase (GGT) activities, whileas hyperin reversed cisplatin-induced such increases. Liver histopathological examination further demonstrated the protection of hyperin against cisplatin-induced liver injury. Further results showed hyperin reversed cisplatin-induced the increase in content of malondialdehyde (MDA) and the decrease in level of total antioxidant capacity (T-AOC) in liver. Moreover, hyperin increased the levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione peroxidase (GPx), glutathione-s transferase (GST) in cisplatininduced liver. Conclusion: Hyperin inhibits cisplatin-induced hepatic oxidative stress, which contributes greatly to the amelioration of cisplatin-induced liver injury in mice.

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“…25,27) Previous studies revealed that polydatin increases autophagy in cardiac cells, multiple myeloma and pancreatic cancer. 28,30) In this study, the expression levels of autophagyassociated proteins in fibroblasts obtained from patients with AS were investigated, including LC3II, Beclin 1 and ATG5. The results demonstrated that treatment with polydatin significantly increased the expression levels of LC3II, Beclin 1 and ATG5 in fibroblasts.…”

Section: Discussionmentioning

confidence: 99%

Polydatin Regulates the Apoptosis and Autophagy of Fibroblasts Obtained from Patients with Ankylosing Spondylitis

Wen

Zhang

et al. 2019

Biological & Pharmaceutical Bulletin

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The development of ankylosing spondylitis (AS) occurs due to excessive proliferation of fibroblasts. Polydatin, a monomeric compound isolated from a traditional Chinese medicine Polygonum cuspidatum, exhibits anti-inflammatory and anti-arthritic effects. However, the mechanisms underlying the regulatory effects of polydatin on the proliferation, apoptosis and autophagy of fibroblasts obtained from patients with AS remain unclear. The aim of this study was to investigate the therapeutic effects of polydatin on symptoms associated with AS. Multiple cellular and molecular biology experiments were performed in the present study, such as cell viability assay, Western blotting, flow cytometry, monodansylcadaverine (MDC) staining and immunofluorescence assays. In the present study, the results revealed that polydatin induced the apoptosis of fibroblasts isolated from patients with AS by upregulating the expression of active caspase-3 and Bax, and downregulating the expression of Bcl-2. Meanwhile, polydatin was revealed to enhance the autophagy of fibroblasts by increasing the expression levels of LC3II, Beclin 1 and Atg5. The results of MDC and immunofluorescence assays further demonstrated that polydatin significantly induced the formation of autophagosomes in fibroblasts. Furthermore, polydatin-induced apoptosis and autophagy were markedly inhibited following treatment with the autophagy inhibitor, 3-methyladenine (3-MA). In conclusion, the results of the present study indicated that polydatin induces the apoptosis and autophagy of fibroblasts obtained from patients suffering from AS, and that polydatin may represent a therapeutic agent for the future treatment of patients with AS.

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The apoptotic and autophagic properties of two natural occurring prodrugs, hyperoside and hypoxoside, against pancreatic cancer cell lines

Cited by 28 publications

References 32 publications

Hyperoside Induces Breast Cancer Cells Apoptosis via ROS-Mediated NF-κB Signaling Pathway

Hyperoside Induces Breast Cancer Cells Apoptosis via ROS-Mediated NF-κB Signaling Pathway

Hyperin protects against cisplatin-induced liver injury in mice

Polydatin Regulates the Apoptosis and Autophagy of Fibroblasts Obtained from Patients with Ankylosing Spondylitis

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