Paeoniflorin inhibition of 6-hydroxydopamine-induced apoptosis in PC12 cells via suppressing reactive oxygen species-mediated PKCδ/NF-κB pathway

Dong, Huijuan; Li, R; Yu, Chunlei; Xu, Tianjiao; Zhang, X; Dong, Miaoxian

doi:10.1016/j.neuroscience.2014.11.008

Cited by 68 publications

(38 citation statements)

References 35 publications

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“…In one scenario, PKCδ could negatively regulate survival signaling in response to apoptotic signals, thus indirectly allowing apoptotic pathways to be activated. In this regard, PKCδ-dependent regulation of MAPK pathways (Efimova, Broome, & Eckert, 2004; Murriel et al, 2004; Blank et al, 2013), PI3K-Akt (Murriel et al, 2004), signal transducer and activator of transcription-1 (STAT-1) (DeVries, Kalkofen, Matassa, & Reyland, 2004), and NFκB (Ren et al, 2014; Dong et al, 2015) has been shown in many contexts. In a second scenario, PKCδ could directly regulate the DNA damage response and cell cycle arrest mechanisms, as discussed above, pushing a cell toward initiation of apoptotic pathways (Bharti et al, 1998; Yoshida et al, 2003; LaGory et al, 2010; Arango et al, 2012; Soriano-Carot et al, 2014).…”

Section: Biological Functions Of Pkcδmentioning

confidence: 99%

Multifunctional roles of PKCδ: Opportunities for targeted therapy in human disease

Reyland

Jones

2016

Pharmacology & Therapeutics

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The serine–threonine protein kinase, protein kinase C-δ (PKCδ), is emerging as a bi-functional regulator of cell death and proliferation. Studies in PKCδ−/− mice have confirmed a pro-apoptotic role for this kinase in response to DNA damage and a tumor promoter role in some oncogenic contexts. In non-transformed cells, inhibition of PKCδ suppresses the release of cytochrome c and caspase activation, indicating a function upstream of apoptotic pathways. Data from PKCδ−/− mice demonstrate a role for PKCδ in the execution of DNA damage-induced and physiologic apoptosis. This has led to the important finding that inhibitors of PKCδ can be used therapeutically to reduce irradiation and chemotherapy-induced toxicity. By contrast, PKCδ is a tumor promoter in mouse models of mammary gland and lung cancer, and increased PKCδ expression is a negative prognostic indicator in Her2+ and other subtypes of human breast cancer. Understanding how these distinct functions of PKCδ are regulated is critical for the design of therapeutics to target this pathway. This review will discuss what is currently known about biological roles of PKCδ and prospects for targeting PKCδ in human disease.

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Section: Biological Functions Of Pkcδmentioning

confidence: 99%

Multifunctional roles of PKCδ: Opportunities for targeted therapy in human disease

Reyland

Jones

2016

Pharmacology & Therapeutics

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“…On the other hand, paeoniflorin has been shown to induce apoptosis in multiple myeloma cells, glioma cells, gastric carcinoma cells, hepatoma cells (HepG2 and SMMC‐7721 cells), cervical cancer cells, and lymphocytes indicating anticancer property of paeoniflorin. Furthermore, paeoniflorin has been showed anti‐apoptotic and pro‐apoptotic effects in differentiated PC12 cells (derived from a pheochromocytoma of the rat adrenal medulla) . However, it remains unknown whether paeoniflorin also affects apoptosis in pituitary tumor cells.…”

Section: Introductionmentioning

confidence: 99%

The prolactin‐release inhibitor paeoniflorin suppresses proliferation and induces apoptosis in prolactinoma cells via the mitochondria‐dependent pathway

Wei

Zhou

Ren

et al. 2018

J of Cellular Biochemistry

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Prolactinomas are the most prevalent functional pituitary adenomas that cause chronic pathological hyperprolactinemia. Prolactin is known to promote cell growth and inhibit apoptosis in cells. Paeoniflorin is the principal component of radix Paeoniae alba (the main ingredient in some traditional herbal formulas clinically used for hyperprolactinemia-associated disorders). Recent findings from intensive studies have suggested that paeoniflorin regulates cell proliferation and apoptosis in many cell lines. However, the effects of paeoniflorin in pituitary tumor cells remain unknown. Here the results by the Cell Counting Kit-8 and colony formation assays showed that paeoniflorin concentration-dependently decreased cell viability in both MMQ and GH3 cells and colony formation in GH3 cells, suggesting inhibition of cell proliferation by paeoniflorin. By flow cytometry, paeoniflorin was found to increase apoptotic rate in MMQ cells. Mechanistically, Western blot results revealed that paeoniflorin enhanced protein expression of cleave caspase-9 and -3, and Bax, whereas it suppressed Bcl-2 protein expression in MMQ cells. Furthermore, paeoniflorin upregulated phosphorylated p53 protein expression, but it decreased prolactin concentration and prolactin protein expression in both MMQ and GH3 cells. Thus, the present results demonstrate that paeoniflorin inhibits cell proliferation and induces the mitochondrial pathway-mediated apoptosis in prolactinoma cells. These antitumor property is associated with inhibition of prolactin secretion. Our findings may provide new insight into the mechanisms underlying improving prolactinoma-associated disorders of paeoniflorin-enriched herbs and formulas.

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“…Previous investigations of the pharmacological effects of paeoniflorin have revealed that paeoniflorin has multiple roles, which include the attenuation of free radical damage, the inhibition of intracellular calcium overload and the abrogation of neurotoxicity (9). In vivo experiments indicate that this has numerous biological effects, including a reduction in blood viscosity and platelet aggregation, dilation of blood vessels, improvement of microcirculation, inhibition of oxidation and action as an anti-convulsive, with low toxicity and few side effects (10).…”

Section: Introductionmentioning

confidence: 99%

Paeoniflorin ameliorates rheumatoid arthritis in rat models through oxidative stress, inflammation and cyclooxygenase 2

Jia

2015

Experimental and Therapeutic Medicine

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Paeoniflorin has anti-inflammatory, anti-allergy, immune regulatory and pain-relieving effects, amongst other roles. However, the mechanisms underlying the protective effects of paeoniflorin on rheumatoid arthritis (RA) remain under investigation; the objective of the current study was to evaluate these protective effects in the context of an RA model. Rats were randomly divided into 5 groups, as follows: The control group, the RA rat model group, and the paeoniflorin groups, in which paeoniflorin was administered at concentrations of 5, 10 and 20 mg/kg for 3 weeks. The pain thresholds and arthritic symptoms of the RA rats were measured. Oxidative stress and inflammatory cytokines were also analyzed and western blot analysis was used to evaluate cyclooxygenase-2 (COX-2) protein expression levels. Paeoniflorin significantly increased the pain threshold and decreased the arthritic symptoms in the RA rat model. Notably, paeoniflorin reduced the malondialdehyde concentration and increased the activity of superoxide dismutase, catalase and glutathione peroxidase. Furthermore, paeoniflorin attenuated the activity of nuclear factor-κB p65 unit, tumor necrosis factor-α, interleukin (IL)-1β and IL-6, and reduced the COX-2 protein expression level. The present study indicates that paeoniflorin ameliorates disease in rat models of RA through oxidative stress, inflammation and alterations to COX-2 expression.

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Paeoniflorin inhibition of 6-hydroxydopamine-induced apoptosis in PC12 cells via suppressing reactive oxygen species-mediated PKCδ/NF-κB pathway

Cited by 68 publications

References 35 publications

Multifunctional roles of PKCδ: Opportunities for targeted therapy in human disease

Multifunctional roles of PKCδ: Opportunities for targeted therapy in human disease

The prolactin‐release inhibitor paeoniflorin suppresses proliferation and induces apoptosis in prolactinoma cells via the mitochondria‐dependent pathway

Paeoniflorin ameliorates rheumatoid arthritis in rat models through oxidative stress, inflammation and cyclooxygenase 2

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