Chrysin sensitizes tumor necrosis factor-α-induced apoptosis in human tumor cells via suppression of nuclear factor-kappaB

Li, Xin; Huang, Qing; Ong, Choon Nam; Yang, Xingfen; Shen, Han‐Ming

doi:10.1016/j.canlet.2010.01.002

Cited by 92 publications

(55 citation statements)

References 41 publications

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“…Thus, inhibition of the release of inflammatory cytokines is an important strategy to protect heart against myocardial damage in T2DM patients. As an important inflammatory cytokine, TNF-α is produced mainly by the activation of monocytes/macrophages, and participates in certain autoimmune diseases (29)(30)(31)(32)(33). Thus, it could stimulate the NO synthase (i-NOS) to synthesize and release a large number of NO.…”

Section: Discussionmentioning

confidence: 99%

Effects of propofol on myocardial ischemia-reperfusion injury in rats with type-2 diabetes mellitus

Wang

et al. 2016

Biomedical Reports

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Abstract. The current study aimed to examine the effects of propofol on myocardial ischemia-reperfusion injury (MIRI) in rats with type-2 diabetes mellitus (T2DM) and to assess the role of inflammatory mediators. Fifty healthy male adult Sprague-Dawley rats were randomly divided into the sham, ischemia-reperfusion (IR), IR plus low, middle and high-dose (6, 12 and 24 mg/kg/h, intravenous) propofol groups. The rats of all the groups were fed a high-sugar and high-fat diet for 8 weeks and streptozotocin (30 mg/kg, intraperitoneally) was used to establish the T2DM model. Apart from the sham group rats, MIRI was induced by ligating the left anterior descending coronary artery for 30 min, followed by reperfusion for 2 h. Heart rate (HR), left ventricular systolic pressure (LVSP), and the rate of left ventricular pressure increase in early systole (± dp/dt max ) were recorded. Levels of cardiac troponin T (cTnT), nitric oxide (NO), endothelin-1 (ET-1), interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were also measured. Myocardial lesions were observed under light microscopy and scanning electron microscopy. Compared with levels prior to arterial occlusion, HR, LVSP, and ± dp/dt max were significantly reduced (P<0.05) following occlusion for 30 min and reper fusion for 2 h. The administration of propofol ameliorated the cardiac function of rats as reflected by the increase in HR, LVSP and ± dp/dt max . In addition, the administration of propofol increased the serum NO concentration, and reduced ET-1 and cTnT levels, as well as levels of inflammatory mediators including IL-1β, IL-6 and TNF-α. Thus, propofol exerts protective effects against MIRI in T2DM rats by increasing NO and reducing ET-1 and the inflammatory mediators.

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Section: Discussionmentioning

confidence: 99%

Effects of propofol on myocardial ischemia-reperfusion injury in rats with type-2 diabetes mellitus

Wang

et al. 2016

Biomedical Reports

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“…Chrysin has been reported to induce apoptosis in a panel of cancer cell lines, including HeLa cervical cancer cells, U937, HL-60 and L1210 leukemia cells (14). Chrysin was also able to inhibit tumor angiogenesis in vivo, which is a key step in cancer cell metastasis (15,16). We previously reported that 7-piperazinethylchrysin (7-PEC) ( Fig.…”

Section: Introductionmentioning

confidence: 99%

Induction of apoptosis by 7-piperazinethylchrysin in HCT-116 human colon cancer cells

et al. 2012

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Abstract. The antitumor activity of 7-piperazinethylchrysin (7-PEC) was investigated in HCT-116 human colon cancer cells. MTT assay revealed that the IC 50 of 7-PEC in HCT-116 cells was 1.5 µM after 72 h of treatment, much lower than that of chrysin (>100 µM). The data showed that 7-PEC was able to inhibit the growth of HCT-116 cells in a concentration-and time-dependent manner. Topical morphological changes of apoptotic body formation after 7-PEC treatment were observed by Hoechst 33258 staining. 7-PEC reduced mitochondrial membrane potential (∆Ψm) of cells in a concentration-dependent manner and increased the production of intracellular reactive oxygen species (ROS). After treatment with 7-PEC, a significant increase of Bax protein expression and decrease of Bcl-2 protein expression were observed at the same time. These events paralleled with activation of p53, caspase-3 and -9 and the release of cytochrome c (cyt-c), as well as poly(ADPribose) polymerase-1 (PARP1) cleavage and downregulation of p-Akt. However, the apoptosis induced by 7-PEC was blocked by Ac-DEVD-CHO, a caspase-3 inhibitor. These results demonstrate that 7-PEC-induced mitochondrial dysfunction in HCT-116 human colon cancer cells triggers events responsible for caspase-dependent apoptosis pathways, and the elevated ratio of Bax/Bcl-2 is likely involved in this effect.

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“…Although chrysin is a natural flavonoid that has been the focus of experimental animal studies in recent years due to its strong antioxidant and anti-inflammatory properties, its protective effect against cisplatin ototoxicity has not been previously evaluated. Chrysin exhibits anti-inflammatory properties by inhibiting NF-K B activation [37]. It was also reported to increase the enzymatic and nonenzymatic antioxidant status, thereby conferring protection against ototoxicity.…”

Section: Discussionmentioning

confidence: 99%

“…Many antioxidant agents have been used to prevent cisplatin-induced ototoxicity in experimental animal or clinical trials [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][33][34][35][36][37]. Kizilay et al [5] performed an experimental study on the protective effect of caffeic acid phenethyl ester (CAPE) on cisplatin ototoxicity and reported that CAPE may have a protective effect.…”

Section: Discussionmentioning

confidence: 99%

The Protective Effect of Chrysin Against Cisplatin İnduced Ototoxicity in Rats

Kelleş

Tan

Kalcıoğlu

et al. 2013

Indian J Otolaryngol Head Neck Surg

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Ototoxicity is a common side effect of cisplatin chemotherapy. The aim of this study was to investigate the potential protective effect of chrysin against cisplatininduced ototoxicity. Thirty-four adult female Wistar albino rats were separated into four groups: a cisplatin group (Group A), with cisplatin administered to ten rats once daily for three consecutive days at doses of 8 mg/kg body weight intraperitoneally (i.p.); a cisplatin plus chrysin group (Group B), with 8 mg/kg of cisplatin administered i.p. daily to ten rats for three consecutive days and 25 mg/kg of chrysin administered via oral gavage in a corn oil for 5 days: a chrysin group (Group C), with 25 mg/kg of chrysin administered via oral gavage in corn oil for 5 days to seven rats; and a control group (Group D), with 5 ml/kg of corn oil administered to seven rats via oral gavage for 5 days. Distortion product otoacoustic emission measurements were performed in the same ear of the rats under general anesthesia at baseline and on the first and fifth days after drug administration. No significant differences were noted between the measurements either in the chrysin group or in the control group. In the cisplatin group, there was a significant worsening of hearing compared to baseline and the measurements on the fifth day at all frequencies. In the statistical analysis, a statistically significant difference was observed at 5039, 6351, 8003, and 10078 Hz frequencies between the measurements on the first and fifth days. In the cisplatin plus chrysin group, there were statistically significant differences at frequencies of 2,003 and 5,039 Hz between the measurements at baseline and on the fifth day, at 3,175 and 5,039 Hz between the measurements on the first and fifth days, and at 8,003 and 100,078 Hz between the measurements at baseline and on the first day. According to these results, this study demonstrates that cisplatin-related ototoxicity can be prevented in rats by the administration of chrysin.

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Chrysin sensitizes tumor necrosis factor-α-induced apoptosis in human tumor cells via suppression of nuclear factor-kappaB

Cited by 92 publications

References 41 publications

Effects of propofol on myocardial ischemia-reperfusion injury in rats with type-2 diabetes mellitus

Effects of propofol on myocardial ischemia-reperfusion injury in rats with type-2 diabetes mellitus

Induction of apoptosis by 7-piperazinethylchrysin in HCT-116 human colon cancer cells

The Protective Effect of Chrysin Against Cisplatin İnduced Ototoxicity in Rats

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