Investigation of effects of newly synthesized Pt(II) complex against human serum albumin and leukemia cell line of K562

Divsalar, Adeleh; Saboury, Ali Akbar; Ahadi, Leila; Zemanatiyar, Elham; Mansouri‐Torshizi, Hassan

doi:10.5483/bmbrep.2010.43.11.766

Cited by 35 publications

(5 citation statements)

References 32 publications

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“…The cells incubated with various concentrations of naringenin were treated with or without 0.5 µg/ml LPS for 24 h and then incubated in 0.5 mg/ml MTT solution. Three hours later, the supernatant was removed and formation of formazan was measured at 540 nm using a microplate reader (26).…”

Section: Methodsmentioning

confidence: 99%

Naringenin attenuates the release of pro-inflammatory mediators from lipopolysaccharide-stimulated BV2 microglia by inactivating nuclear factor-κB and inhibiting mitogen-activated protein kinases

Choi¹

2012

Int J Mol Med

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Abstract. Naringenin, one of the most abundant flavonoids in citrus fruits and grapefruits, has been reported to exhibit anti-inflammatory and antitumor activities. However, the cellular and molecular mechanisms underlying the naringenin anti-inflammatory activity are poorly understood. In this study, we conducted an investigation of the inhibitory effects of naringenin on the production of lipopolysaccharide (LPS)-induced pro-inflammatory mediators in BV2 microglial cells. We found that pre-treatment with naringenin prior to treatment with LPS significantly inhibited excessive production of nitric oxide (NO) and prostaglandin E 2 (PGE 2 ) in a dose-dependent manner. The inhibition was associated with downregulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression. Naringenin also attenuated the production of pro-inflammatory cytokines and chemokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein-1 (MCP-1) by suppressing expression of mRNAs for these proteins. In addition, the molecular mechanism underlying naringenin-mediated attenuation in BV2 cells has a close relationship to suppressing translocation of the nuclear factor-κB (NF-κB) p65 subunit into the nucleus and the phosphorylation of Akt and mitogen-activated protein kinases (MAPKs). These findings suggest that naringenin may provide neuroprotection through suppression of pro-inflammatory pathways in activated BV2 microglial cells.

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Section: Methodsmentioning

confidence: 99%

Naringenin attenuates the release of pro-inflammatory mediators from lipopolysaccharide-stimulated BV2 microglia by inactivating nuclear factor-κB and inhibiting mitogen-activated protein kinases

Choi¹

2012

Int J Mol Med

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“…This dependence was, therefore, analyzed in order to better characterize the forces acting between ligand (ZnO nanoparticles) and protein (proteinase K). 57 Essentially, there are four types of nano-covalent interactions stabilizing ligands bound to proteins: hydrogen bonds, electrostatic forces, van der Waals forces and hydrophobic interactions. 58 The thermodynamic parameters (DG , DH and DS ) are very important for interpreting the binding modes.…”

Section: Fluorescence Quenching Of Proteinase Kmentioning

confidence: 99%

Green synthesis of zinc oxide nanoparticles and their effect on the stability and activity of proteinase K

et al. 2016

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“…The cells incubated with various concentrations of 7,8-DHF were treated with or without 0.5 µg/ml LPS for 24 h, and then incubated in 0.5 mg/ml MTT solution. Three hours later, the supernatant was removed and formation of formazan was measured at 540 nm using a microplate reader (31).…”

Section: Methodsmentioning

confidence: 99%

7,8-Dihydroxyflavone exhibits anti-inflammatory properties by downregulating the NF-κB and MAPK signaling pathways in lipopolysaccharide-treated RAW264.7 cells

et al. 2012

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Abstract. 7,, a member of the flavonoid family, has received considerable attention as a selective tyrosine kinase receptor B agonist. Several studies have indicated that 7,8-DHF has neurotrophic and antioxidant activities. However, little is known about the cellular and molecular mechanisms underlying the anti-inflammatory activity of 7,8-DHF. Therefore, we investigated whether 7,8-DHF affects the expression of inflammatory mediators in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Our results indicated that 7,8-DHF significantly attenuated secretion of LPS-induced inflammatory mediators nitric oxide (NO), prostaglandin E 2 (PGE 2 ) and interleukin-1β (IL-1β) in RAW264.7 cells. Additionally, LPS-induced expression of inducible NO synthase (iNOS), cyclooxygenase (COX)-2 and IL-1β was decreased by pre-treatment with 7,8-DHF. Our results also showed that 7,8-DHF reduces LPS-induced nuclear factor-κB (NF-κB) activity via the suppression of the nuclear translocation of NF-κB p65 and the degradation of inhibitor κB (lκB). In addition, 7,8-DHF inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs) such as extracellular-signal-related kinase (ERK), p38, and c-Jun N-terminal kinase (JNK). These results suggest that the anti-inflammatory property of 7,8-DHF is related to the downregulation of iNOS, COX-2 and IL-1β, due to NF-κB inhibition as well as to the negative regulation of MAPK activation in RAW264.7 cells. Thus, 7,8-DHF may be a novel therapeutic agent for the prevention of various inflammatory diseases.

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Investigation of effects of newly synthesized Pt(II) complex against human serum albumin and leukemia cell line of K562

Cited by 35 publications

References 32 publications

Naringenin attenuates the release of pro-inflammatory mediators from lipopolysaccharide-stimulated BV2 microglia by inactivating nuclear factor-κB and inhibiting mitogen-activated protein kinases

Naringenin attenuates the release of pro-inflammatory mediators from lipopolysaccharide-stimulated BV2 microglia by inactivating nuclear factor-κB and inhibiting mitogen-activated protein kinases

Green synthesis of zinc oxide nanoparticles and their effect on the stability and activity of proteinase K

7,8-Dihydroxyflavone exhibits anti-inflammatory properties by downregulating the NF-κB and MAPK signaling pathways in lipopolysaccharide-treated RAW264.7 cells

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