Resveratrol exerts an anti-apoptotic effect on human bronchial epithelial cells undergoing cigarette smoke exposure

Zhang, Li; Guo, Xiang; Xie, Wang; Li, Yuping; Ma, Mengqing; Tan, Yuan; Luo, Bailing

doi:10.3892/mmr.2014.2925

Cited by 37 publications

(30 citation statements)

References 27 publications

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“…Further, resveratrol is known to activate SIRT1 which in turn specifically regulates expression of MMP-9 via NFκB pathway [43]. In our study, the significant inhibition of MMP-9 activity achieved with the combination of resveratrol (50 mg/kg) and dexamethasone (2.5 mg/kg) can also be attributed to SIRT1 activation potential of resveratrol.…”

Section: Discussionsupporting

confidence: 51%

Resveratrol potentiates the effect of dexamethasone in rat model of acute lung inflammation

Sadarani

Majumdar

2015

International Immunopharmacology

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Section: Discussionsupporting

confidence: 51%

Resveratrol potentiates the effect of dexamethasone in rat model of acute lung inflammation

Sadarani

Majumdar

2015

International Immunopharmacology

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“…The 8% RBCs were stained using 0.25 mg/ml Hoechst dye for 10 min at 37°C. The cells (10 l) were then observed under a fluorescence microscope (IX71; Olympus, Tokyo, Japan), and the WBCs were counted (28).…”

Section: Neutralization Of Lpsmentioning

confidence: 99%

Antimicrobial Peptide CMA3 Derived from the CA-MA Hybrid Peptide: Antibacterial and Anti-inflammatory Activities with Low Cytotoxicity and Mechanism of Action in Escherichia coli

Lee

Seo

Luchian

et al. 2016

Antimicrob Agents Chemother

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dCA-MA is a hybrid antimicrobial peptide (AMP) derived from two naturally occurring AMPs, cecropin A and magainin 2. CA-MA shows strong antimicrobial activity against Gram-negative and Gram-positive bacteria but also exhibits cytotoxicity toward mammalian cells. Our objective was to identify CA-MA analogues with reduced cytotoxicity by systematic replacement of amino acids with positively charged R groups (His and Lys), aliphatic R groups (Leu), or polar R groups (Glu). Among the CA-MA analogues studied (CMA1 to -6), CMA3 showed the strongest antimicrobial activity, including against drug-resistant Escherichia coli and Pseudomonas aeruginosa strains isolated from hospital patients. CMA3 appeared to act by inducing pore formation (toroidal model) in the bacterial membrane. In cytotoxicity assays, CMA3 showed little cytotoxicity toward human red blood cells (hRBCs) or HaCaT cells. Additionally, no fluorescence was released from small or giant unilamellar vesicles exposed to 60 M CMA3 for 80 s, whereas fluorescence was released within 35 s upon exposure to CA-MA. CMA3 also exerted strong lipopolysaccharide (LPS)-neutralizing activity in RAW 264.7 cells, and BALB/c mice exposed to LPS after infection by Escherichia coli showed improved survival after administration of one 0.5-mg/kg of body weight or 1-mg/kg dose of CMA3. Finally, in a mouse model of septic shock, CMA3 reduced the levels of proinflammatory factors, including both nitric oxide and white blood cells, and correspondingly reduced lung tissue damage. This study suggests that CMA3 is an antimicrobial/antiendotoxin peptide that could serve as the basis for the development of anti-inflammatory and/or antimicrobial agents with low cytotoxicity. W hen microorganisms infect vertebrate or invertebrate animals, the secretion of cytokines, chemokines, and other peptides is an important component of the animals' innate immune response (1, 2). Among those other peptides are antimicrobial peptides (AMPs), which play key roles in the innate immune responses of mammals, amphibians, and insects, among others (3, 4). Indeed, more than 2,300 different AMPs have been identified and isolated from a wide range of organisms, including bacteria (n ϭ 322), protozoa (n ϭ 6), fungi (n ϭ 12), plants (n ϭ 306), and animals (n ϭ 1,801). Most AMPs contain at least 10 amino acid residues, have a net charge ranging from Ϫ3 to ϩ20, and exhibit Ͻ60% hydrophobicity (5). Together, these features underlie the bactericidal activity of AMPs, enabling them to bind and form damaging pores in the membranes of Gram-negative and Gram-positive bacteria. To induce pore formation, AMPs have an ␣-helical structure and the ability to interact with anionic components of the cytoplasmic membrane, resulting in the formation of toroidal, carpet, or barrel stave pores (6). Additionally, many AMPs can potentially prevent septic shock via their antiendotoxic activity through electrostatic interaction with lipopolysaccharides (LPS) and lipoteichoic acid in the bacterial membrane (7-9).CA-MA is a hybrid AMP syn...

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“…Additionally, there have been reports that resveratrol can sensitise cancer cells to cytostatics in various types of chemotherapy resistance. Very low toxicity and protective effect on normal cells are additional values of this polyphenol (13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

Classical and atypical resistance of cancer cells as a target for resveratrol

et al. 2016

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The phenomenon of cancer cell resistance to chemotherapeutics is the main cause of insensitivity to anticancer therapy. Thus, the current challenge remains searching for substances sensitising the activity of cytostatic drugs. In this respect, resveratrol is a very promising therapeutic agent. It has pleiotropic effect on cancer cells, which can play a key role in numerous resistance mechanisms, both classical and atypical. The purpose of the present study was to assess the effect of resveratrol on the inhibition of human pancreatic cancer cell proliferation and on the level of cytostatic resistance-associated proteins. The study was performed on human pancreatic cancer cell lines EPP85-181P (control), EPP85-181RDB (daunorubicin resistance) and EPP85-181PRNOV (mitoxantrone resistance). The effect of resveratrol on the viability and proliferation of the studied cell lines was evaluated by SRB assay, whereas cell cycle arrest and cytostatic accumulation by FACS. Western blot analysis was used to determine the level of P-glycoprotein, topoisomerase II α and β and immunofluorescence technique to visualise the proteins in the cells. Resveratrol inhibited proliferation of all studied cell lines. Phase-specific cell cycle arrest depended on the type of cancer cells. Resveratrol decreased the level and activity of P-gp in EPP85-181RDB cells. In EPP85-181PRNOV cells, expression of both TopoII isoforms increased in a statistically significant manner. The results of in vitro studies support the possibility of potential use of resveratrol in breaking cancer cell resistance to chemotherapeutic drugs.

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Resveratrol exerts an anti-apoptotic effect on human bronchial epithelial cells undergoing cigarette smoke exposure

Cited by 37 publications

References 27 publications

Resveratrol potentiates the effect of dexamethasone in rat model of acute lung inflammation

Resveratrol potentiates the effect of dexamethasone in rat model of acute lung inflammation

Antimicrobial Peptide CMA3 Derived from the CA-MA Hybrid Peptide: Antibacterial and Anti-inflammatory Activities with Low Cytotoxicity and Mechanism of Action in Escherichia coli

Classical and atypical resistance of cancer cells as a target for resveratrol

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