Puerarin induces cell apoptosis in human chondrosarcoma cell line SW1353 via inhibition of the PI3K/Akt signaling pathway

Huang, Li; Cao, Junqing; Cao, Lan; Gao, Ling; Yang, Ying; Xu, Li

doi:10.3892/ol.2017.6901

Cited by 12 publications

(11 citation statements)

References 25 publications

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“…The results of the present study indicate that Puerarin significantly suppressed PI3K, p-Akt and p-mTOR protein expression in HeLa HPV-18 positive cervical cancer cells, thereby reducing their proliferative and migration abilities; however, PI3K upregulation reduced the anticancer effect of Puerarin on HeLa cells. Huang et al (13) revealed that Puerarin induces cell apoptosis in human chondrosarcoma cells via inhibition of the PI3K/Akt signaling pathway, which supports the results of the present study.…”

Section: Discussionsupporting

confidence: 92%

“…Puerarin has strong pharmacological activity (12) and a wide range of pharmacological effects, including anti-arrhythmia, anti-myocardial infarction, anti-angiectasis, antitumor, microcirculation improvement, blood fat reduction, increased cerebral blood flow, protection against oxidation, regulation of bone metabolism and reduction of intraocular pressure (11,12). Huang et al (13) demonstrated that Puerarin induces cell apoptosis in human chondrosarcoma cells via inhibiting the PI3K/Akt signaling pathway. The aim of the present study was to explore the effects of Puerarin on apoptosis in HPV-positive cervical cancer cells and the molecular mechanisms responsible.…”

Section: Introductionmentioning

confidence: 99%

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Puerarin suppresses cell growth and migration in HPV‑positive cervical cancer cells by inhibiting the PI3K/mTOR signaling pathway

Lee

Yang

et al. 2019

Exp Ther Med

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Puerarin is an effective component that is present in high concentrations in the Pueraria lobata plant and is extensively distributed throughout nature. Puerarin possesses a number of pharmacological effects and has strong pharmacological activity with few side effects and extensive clinical applications. The aim of the present study was to explore the effects of Puerarin on the apoptosis of human papillomavirus (HPV)-positive cervical cancer cells and the underlying molecular mechanisms. MTT assay, lactate dehydrogenase activity and Annexin V/fluorescein isothiocyanate/propidium iodide analysis were used to analyze cell growth of HPV-positive HeLa cervical cancer cells treated with Puerarin. Western blotting was performed to measure protein expression in the treated cells. Puerarin significantly reduced cell proliferation and induced apoptosis in HeLa cells. In addition, it was observed that Puerarin significantly enhanced caspase-3/9 activities and significantly increased B-cell lymphoma 2-asscoiate X protein expression in HeLa cells. Puerarin suppressed phosphatidylinositol-3 kinase (PI3K), phosphorylated (p)-protein kinase B (Akt) and p-mammalian target of rapamycin (mTOR) protein expression in HeLa cells. These results indicate that Puerarin induces apoptosis in HPV-positive HeLa cervical cancer cells via inhibiting PI3K/Akt/mTOR signaling.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Puerarin suppresses cell growth and migration in HPV‑positive cervical cancer cells by inhibiting the PI3K/mTOR signaling pathway

Lee

Yang

et al. 2019

Exp Ther Med

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“…Phosphoinositide 3-kinase (PI3K), a member of the phospholipid kinase family, serves important roles in the regulation of the apoptosis, proliferation, differentiation and metabolism of cells (9). The serine-threonine protein kinase Akt is a downstream target of PI3K; when stimulated by extracellular signals, PI3K-activated Akt initiates a cascade of intracellular reactions (10). PI3K is composed of a regulatory subunit (p85) and a catalytic subunit (p110), and activation of the catalytic subunit depends upon the phosphorylation of p85 (11).…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rb1 attenuates intestinal ischemia/reperfusion‑induced inflammation and oxidative stress via activation of the PI3K/Akt/Nrf2 signaling pathway

Chen

Wang

et al. 2019

Mol Med Report

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Ginsenoside Rb1 (GRb1), one of the major active saponins isolated from ginseng, has recently been reported to protect various organs against ischemia/reperfusion (IR) injury; however, the mechanisms underlying these protective effects following intestinal IR (IIR) remain unclear. The present study aimed to evaluate the effects of GRb1 on IIR injury and determine the mechanisms involved in these effects. Sprague Dawley rats were subjected to 75 min of superior mesenteric artery occlusion, followed by 3 h of reperfusion. GRb1 (15 mg/kg) was administered intraperitoneally 1 h prior to the induction of IIR, with or without intravenous administration of Wortmannin [WM; a phosphoinositide 3-kinase (PI3K) inhibitor, 0.6 mg/kg]. The degree of intestinal injury and oxidative stress-induced damage was determined by histopathologic evaluation and measurement of the serum activity levels of D-lactate, diamine oxidase and endotoxin, and the levels of malondialdehyde (MDA), superoxide dismutase (SOD) and 8-iso-prostaglandin F 2α (8-iso-PGF 2α ). The protein expression levels of p85, phosphorylated (p)-p85, protein kinase B (Akt), p-Akt and nuclear factor erythroid 2-related factor 2 (Nrf2) were determined via western blotting, and the concentrations of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 were measured via ELISA. It was revealed that IIR led to severe intestinal injury (as determined by significant increases in intestinal Chiu scores), which was accompanied with disruptions in the integrity of the intestinal mucosal barrier. IIR also increased the expression levels of TNF-α, IL-1β, IL-6, MDA and 8-iso-PGF 2α in the intestine, and decreased those of SOD. GRb1 reduced intestinal histological injury, and suppressed inflammatory responses and oxidative stress. Additionally, the protective effects of GRb1 were eliminated by WM. These findings indicated that GRb1 may ameliorate IIR injury by activating the PI3K/protein kinase B/Nrf2 pathway.

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“…miR-155 mimic (100 ng), miR-155 inhibitor (100 ng) and negative control (100 ng) were transfected into cells using Lipofectamine 2000 (Thermo Fisher Scientific, Inc.). Following transfection for 6 h, the medium was removed and fresh medium was added, containing 0.1 ng/ml human interleukin (IL)-4 (Sigma-Aldrich; Merck KGaA), 1 ng/ml human tumor necrosis factor (TNF)-α (Sigma-Aldrich; Merck KGa A) a nd 10 ng/m l huma n inter feron ( I F N )-γ (Sigma-Aldrich; Merck KGaA) for 24 h. Cells were then cultured as keratinocyte-induced HacaT cells, an in vitro model for psoriasis, as previously reported in the literature (14). cells were induced with 100 ng/ml LPS (Beyotime Institute of Biotechnology, Jiangsu, china) for 24 h. cells were treated with NLRP3 inhibitor, Mcc950 (2 nM; MedChemExpress, Shanghai, China) for 8 h.…”

Section: Methodsmentioning

confidence: 99%

Silencing of miR‑155 suppresses inflammatory responses in psoriasis through inflammasome NLRP3 regulation

Luo

Zeng

et al. 2018

Int J Mol Med

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Psoriasis is a dermatosis with the major clinical symptoms of scale, erythema and itching, and it has a long disease course. In addition, it is easily recurrent and refractory, greatly affecting the physical and mental health of patients. In the present study, it was hypothesized that the function of miR‑155 increases psoriasis‑induced inflammation and that its expression may be dependent on inflammasome activation. miR‑155 expression was examined by gene chip array and quantitative polymerase chain reaction analysis. miR‑155 expression levels were significantly increased in an in vivo model of psoriasis compared with normal tissues, as was the expression of NLR family pyrin domain containing 3 (NLRP3). In vitro, using keratinocyte‑induced HaCaT cells as a model for psoriasis, silencing of miR‑155 was confirmed to significantly decrease inflammation and NLRP3/caspase‑1 signaling. Activation of toll‑like receptor 4 (TLR4) enhanced the miR‑155‑induced inflammatory response in the in vitro keratinocyte model. Treatment with a TLR4 inhibitor or an NLRP3 inhibitor reversed the miR‑155‑mediated inflammation in the same cell system. The present study demonstrated that miR‑155 silencing suppressed psoriasis‑associated inflammatory responses through inflammasome NLRP3 regulation.

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Puerarin induces cell apoptosis in human chondrosarcoma cell line SW1353 via inhibition of the PI3K/Akt signaling pathway

Cited by 12 publications

References 25 publications

Puerarin suppresses cell growth and migration in HPV‑positive cervical cancer cells by inhibiting the PI3K/mTOR signaling pathway

Puerarin suppresses cell growth and migration in HPV‑positive cervical cancer cells by inhibiting the PI3K/mTOR signaling pathway

Ginsenoside Rb1 attenuates intestinal ischemia/reperfusion‑induced inflammation and oxidative stress via activation of the PI3K/Akt/Nrf2 signaling pathway

Silencing of miR‑155 suppresses inflammatory responses in psoriasis through inflammasome NLRP3 regulation

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