Anti-inflammatory Effects Of Resveratrol Research Articles

Resveratrol as a potential protective compound against metabolic inflammation

Although the exact mechanism linking obesity to type 2 diabetes (T2D) remains unknown, accumulating evidence suggests that low-grade chronic metabolic inflammation or ‘metainflammation’ plays a pivotal role. Adipose tissue is the primary site of meta-inflammation, and overproduction of pro-inflammatory cytokines in this tissue affects other organs such as the liver, skeletal muscle, pancreas, and brain. This leads to the development of insulin resistance and metabolic irregularities in these tissues. Therefore, strategies targeting metainflammation could be effective in treating T2D and related metabolic traits. Resveratrol, a polyphenol, is suggested to possess anti-inflammatory and immunomodulatory activities. The anti-inflammatory effect of resveratrol is mediated through several mechanisms including the suppression of nuclear factor kB (NF-kB), down-regulation of extracellular signal-regulated kinase (ERK)/p38 mitogen-activated protein kinase (MAPK) signaling, suppression of toll-like receptor (TLR)-mediated pathway; inhibition of NLR family pyrin domain containing 3 (NLRP3) inflammasome activation, reduction of reactive oxygen species (ROS) generation, suppression of immune cell infiltration into tissues; and inhibition of pro-inflammatory cytokines production. This review will examine the evidence on the role of resveratrol in modulating inflammation in various organs affected by obesity such as liver, skeletal muscle, kidney, heart and brain

Resveratrol has its antioxidant and anti-inflammatory protective mechanisms decreased in aging

In the elderly, there is an increase in oxidative and inflammatory activity. Resveratrol (RSV) is a polyphenol that has several proven biological activities, such as antioxidant and anti-inflammatory. Thus, the aim of our study was to verify the possible antioxidant and anti-inflammatory effects of RSV on human mononuclear cells (PBMCs) from donors aged between 40 and 59 and 60–80 years old. For this, 6–8 patients were selected by age group. Cells were isolated and divided into 4 groups: Control (C), RSV only, H2O2 (to induce an oxidizing environment – C+) and H2O2+RSV. The quantification of reactive nitrogen species (NO and ONOO-), as well as pro and anti-inflammatory cytokines (TNFα, IL-6 and IL-10) was performed. Pearson's correlation and comparison between groups were performed (p<0.05). Our results showed a greater role of RSV in the middle-aged compared to the elderly group, in relation to the balance of NO/ONOO- and the levels of cytokines IL-6 and TNFα. It was also possible to observe an improvement in the anti-inflammatory profile in both age groups, but more effective in the cells in the middle-aged group. Thus, we could observe that RSV has better activity in the reduction of important biomarkers of oxidation and inflammation.

Healing effects of monomer and dimer resveratrol in a mouse periodontitis model

BackgroundThe antioxidant and anti-inflammatory effects of resveratrol have been reported previously. Particularly, monomeric trans-resveratrol has been demonstrated to produce positive effects in various pathological processes. We reported previously that resveratrol dimer-rich melinjo extract, among others, caused bone healing, decreased local oxidative damage, and activated antioxidants nuclear factor erythroid 2-related factor 2 (Nrf2) pathways in a mouse model of experimentally induced periodontitis (EP). This study aimed to compare the bone-healing effects of the resveratrol monomer to the resveratrol dimer (gnetin C found in melinjo seed extract) in a model of EP and investigate the involvement of Nrf2 for effects of either form of resveratrol.MethodsEP was induced experimentally in mice by placement of a 9 − 0 silk ligature around the left second molar. Mice received 10 mg/kg of either resveratrol monomer or dimer intraperitoneally on day 15 after induction of EP. The bone level around the ligated teeth was measured over time, and levels of proinflammatory cytokines and oxidative stress were measured in the periodontal tissues around the ligated teeth.ResultsResveratrol dimer induced greater periodontal bone healing as compared to that related to use of the resveratrol monomer. It appears that healing of periodontal bone in either group was likely related to master regulation of antioxidant nuclear factor erythroid 2-related factor 2 (Nrf2) significantly. Downregulation of IL-1β, a proinflammatory cytokine was also demonstrated in the resveratrol dimer group.ConclusionOur results showed that administration of resveratrol in either dimer form or the monomeric form reduced periodontal bone loss with greater inhibition of bone loss being demonstrated in the dimer group as compared to the monomer group and that these effects were related in all likelihood to decreased oxidative stress and hence reduction in local inflammation.

Resveratrol Attenuates Mast Cell Mediated Allergic Reactions: Potential for Use as a Nutraceutical in Allergic Diseases?

Allergic diseases are one of the most common health disorders affecting about 30% of the world population. Mast cells (MCs) are key effector cells of allergic reactions by releasing proinflammatory mediators including histamine, lipid mediators, and cytokines/chemokines. Natural substances like secondary plant substances such as resveratrol (RESV), which can contribute to prevention and treatment of diseases, are becoming increasingly interesting for use as nutraceuticals. In this review, the anti-inflammatory effects of RESV on MC-mediated allergic reactions in vitro and in vivo models are summarized. The studies indicate that RESV inhibits MC degranulation, synthesis of arachidonic acid metabolites, expression of cytokines and chemokines as well as activation of signal molecules involved in proinflammatory mechanisms. Also, beneficial impacts by this polyphenol are reported in randomized controlled trials with allergic rhinitis patients. Although it cannot yet be concluded that RESV can be used successfully in allergy patients in general, there are many results that indicate a possible role for RESV for use as an anti-inflammatory nutraceutical. However, strategies to favorably influence the poor bioavailability of RESV would be helpful.

Histomorphological changes and molecular mechanisms underlying the ameliorative effect of resveratrol on the liver of silver nanoparticles-exposed rats

ABSTRACT Exposure to the deleterious effects of silver nanoparticles (AgNPs) is inevitable due to their wide use in medicine and daily life. The current study aimed to delineate the histomorphological changes and the molecular mechanisms underlying the ameliorative effect of Resveratrol (RSV) on rats’ livers exposed to AgNPs. Fifty healthy adult male Wistar albino rats were divided into four groups: control, AgNPs-exposed, RSV-treated after AgNPs exposure, and recovery groups. Liver sections were examined by light and electron microscopes, and immunohistochemistry was performed for detection of activated caspase3 and TNFα. Serum ALT and AST, plasma levels of TNFα, IL-6, GSH and SOD were measured. mRNA expression of SIRT1, ADORA3, PAI, CDK1, Nrf2 and NFκB genes in liver tissue homogenate was performed using qRT-PCR. AgNPs-exposure for 28 days caused marked liver tissue damage with trapping in hepatocytes and Kupffer cells, while RSV treatment ameliorated liver ultrastructure and function. Our results clarified the molecular basis of RSV ameliorative effect on liver tissue by significant upregulation of SIRT1-NrF2 signaling pathway with increased levels of the antioxidant GSH and SOD, which represent the antioxidant effect of RSV. Significant upregulation of the protective ADORA3 with downregulation of the proinflammatory PAI-1 and NFκB mRNA expression levels besides decreased plasma levels of TNFα, IL-6 and decreased immunoexpression of TNFα in liver tissue, represent the anti-inflammatory effect of RSV. In addition, decreased immunoexpression of caspase3 and downregulation of CDK1 expression, represent its antiapoptotic effect. In conclusion: RSV ameliorates AgNPs-induced liver damage by antioxidant, anti-inflammatory and antiapoptotic effects. Abbreviations: AgNPs: Silver nanoparticles, RSV: Resveratrol, ROS: Reactive oxygen species, ESR: Electron spin resonance, DMPO: 5,5-Dimethyl-1-pyrroline-N-oxide, H2O2: Hydrogen peroxide, SOD: Superoxide dismutase, CAT: Catalase, GPx: Glutathione peroxidase, MPTP: Methyl-4-phenyl-1.2.3.6-tetrahydropyridine, MDA: Malondialdehyde, TNF: Tumor necrosis factor, GSH: Glutathione, Nrf2: Nuclear factor-erythroid 2-related factor 2, ARE: Antioxidant response elements, KEAP1: Kelch-1ike ECH-associated protein l, AMPK: AMP-activated protein kinase, HO-1: Heme oxygenase-1, NF-κB: Nuclear factor-kappa B, SIRT1: Sirtuins, FOXO: Forkhead box, UCP2: Uncoupling protein 2, STZ: Streptozotocin nicotinamide, HSC: hepatic stellate cells, ECM: extracellular matrix.

Evaluation of antioxidant and anti-inflammatory effect of Resveratrol and BioPerine combination

Evaluation of antioxidant and anti-inflammatory effect of Resveratrol and BioPerine combination

Synergistic anti-inflammatory effects of resveratrol and vitamin E in lipopolysaccharide-induced RAW264.7 cells

Synergistic anti-inflammatory effects of resveratrol and vitamin E in lipopolysaccharide-induced RAW264.7 cells

Anti-Inflammatory Effects of Resveratrol on Human Retinal Pigment Cells and a Myopia Animal Model.

Resveratrol is a key component of red wine and other grape products. Recent studies have characterized resveratrol as a polyphenol, and shown its beneficial effects on cancer, metabolism, and infection. This study aimed to obtain insights into the biological effects of resveratrol on myopia. To this end, we examined its anti-inflammatory influence on human retinal pigment epithelium cells and in a monocular form deprivation (MFD)-induced animal model of myopia. In MFD-induced myopia, resveratrol increased collagen I level and reduced the expression levels of matrix metalloproteinase (MMP)2, transforming growth factor (TGF)-β, and nuclear factor (NF)-κB expression levels. It also suppressed the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β. Resveratrol exhibited no significant cytotoxicity in ARPE-19 cells. Downregulation of inflammatory cytokine production, and inhibition of AKT, c-Raf, Stat3, and NFκB phosphorylation were observed in ARPE-19 cells that were treated with resveratrol. In conclusion, the findings suggest that resveratrol inhibits inflammatory effects by blocking the relevant signaling pathways, to ameliorate myopia development. This may make it a natural candidate for drug development for myopia.

Anti-allergic and anti-inflammatory effects of resveratrol via inhibiting TXNIP-oxidative stress pathway in a mouse model of allergic rhinitis

BackgroundAllergic rhinitis (AR) is a type I hypersensitivity mediated by IgE in the nose. Thioredoxin-interacting protein (TXNIP) plays a pivotal role in the process of producing reactive oxygen species (ROS). Resveratrol is a TXNIP inhibitor. Nonetheless, its role and mechanism in AR are still undetermined. The present study aimed to explore the effect and mechanism of resveratrol on an ovalbumin (OVA) induced mouse model of AR. MethodsAR murine model was established using OVA and administrated intranasally with resveratrol or N-acetylcysteine (NAC). Hematoxylin and eosin (HE) stain was used for evaluating eosinophils. Immunohistochemistry (IHC) staining and real-time PCR were employed to evaluate immunolabeling and mRNA expression of TXNIP in nasal mucosas of mice. Malondialdehyde (MDA) level and superoxide dismutase (SOD) activity in nasal tissue homogenates were measured using MDA and SOD Assay Kit. Concentrations of OVA-specific IgE and histamines in serum, and OVA-specific IgE, PGD2, LTC4, ECP, IL-4, IL-5, IL-6, IL-33 and TNF-α in nasal lavage fluid (NLF) were assayed by ELISA. In vitro studies, western blotting, real-time PCR, ELISA, ROS detecting dye DCFH-DA, MDA, and SOD Assay Kit were performed to evaluate the effects and mechanisms of OVA, resveratrol or NAC on spleen mononuclear cells. ResultsWe found significant alternations of sneezing, nasal rubbing, inflammatory cytokines, eosinophil numbers, TXNIP, MDA, and SOD levels in resveratrol or NAC treated mice compared with untreated AR mice. In cultured spleen mononuclear cells, TXNIP, MDA, SOD, ROS and inflammatory cytokines levels were altered by OVA but reversed by resveratrol or NAC. ConclusionsResveratrol could effectively alleviate murine AR by inhibiting TXNIP-oxidative stress pathway.

Preparation, Characterization, and In Vitro Sustained Release Profile of Resveratrol-Loaded Silica Aerogel.

Silica aerogel, a kind of nanoporous material, is regarded as a desired drug carrier for its low toxicity, high specific surface area, and excellent biocompatibility. Using silica aerogel in a drug carrier may be an appropriate method to improve the performance of pure resveratrol. In this study, resveratrol-loaded silica aerogel (RSA) as a drug delivery system was prepared by the sol-gel method. Before gelling, resveratrol was added into the hydrolyzed tetraethyl orthosilicate (TEOS) ethanol solution then dispersed by stir and ultrasound. The results showed that RSA has a high loading rate of 19% with low cost and excellent biocompatibility. The SEM images showed that silica aerogel wraps up outside the resveratrol. Sustained releasing effect could be observed in RSA after 1 h, while pure resveratrol did not display this. The release of RSA lasted for over 6 h, and the release amount reached over 90% and 80% in either simulated gastric fluid (pH = 2.0) or phosphate-buffered saline (pH = 7.4) at 37 °C. Preliminary in vitro toxicity test revealed RSA to be biocompatible and stable; and when coupled with the anti-inflammatory effects of resveratrol, showed good potential for osteoarthritis treatment.

Role of Resveratrol in Modulating microRNAs in Human Diseases: From Cancer to Inflammatory Disorder.

Cancer and inflammatory disorders are two important public health issues worldwide with significant socio.economic impacts. Despite several efforts, the current therapeutic platforms are associated with severe limitations. Therefore, developing new therapeutic strategies for the treatment of these diseases is a top priority. Besides current therapies, the utilization of natural compounds has emerged as a new horizon for the treatment of cancer and inflammatory disorders as well. Such natural compounds could be used either alone or in combination with the standard cancer therapeutic modalities such as chemotherapy, radiotherapy, and immunotherapy. Resveratrol is a polyphenolic compound that is found in grapes as well as other foods. It has been found that this medicinal agent displays a wide pharmacological spectrum, including anti-cancer, anti-inflammatory, anti-microbial, and antioxidant activities. Recently, clinical and pre-clinical studies have highlighted the anti-cancer and anti-inflammatory effects of resveratrol. Increasing evidence revealed that resveratrol exerts its therapeutic effects by targeting various cellular and molecular mechanisms. Among cellular and molecular targets that are modulated by resveratrol, microRNAs (miRNAs) have appeared as key targets. MiRNAs are short non-coding RNAs that act as epigenetic regulators. These molecules are involved in many processes that are involved in the initiation and progression of cancer and inflammatory disorders. Herein, we summarized various miRNAs that are directly/indirectly influenced by resveratrol in cancer and inflammatory disorders.

Resveratrol attenuates the MSU crystal-induced inflammatory response through the inhibition of TAK1 activity

TAK1 is closely associated with the NF-κB and MAPK signaling pathways. In the present study, we aimed to explore the relationship between TAK1 and gout as well as the effects of resveratrol on TAK1 activity and MSU crystal-induced inflammation. The expression levels of total TAK1 and phosphorylated TAK1 in gout patients were detected by western blotting. The influence of resveratrol on TAK1 activity and MSU crystal-induced inflammation was investigated in THP-1 cell and murine models of gout. The results showed that TAK1 and p-TAK1 were highly expressed in gouty arthritis patients. MSU crystals accelerated the expression of TAK1 and p-TAK1 in human PBMCs. The anti-inflammatory effects of resveratrol on MSU crystal-induced inflammation in vitro and in vivo included the alleviation of pro-inflammatory cytokines, inflammatory cell recruitment and foot swelling. Resveratrol limited the activation of TAK1 and its downstream signaling pathway, including the degradation of IκBα, the activation of NF-κB P65 and the phosphorylation of P38 and JNK. In conclusion, resveratrol may have a potential therapeutic effect on gouty arthritis by inhibiting TAK1 activity.

Anti-Inflammatory Effects of Resveratrol: Mechanistic Insights.

Inflammation is the principal response invoked by the body to address injuries. Despite inflammation constituting a crucial component of tissue repair, it is well known that unchecked or chronic inflammation becomes deleterious, leading to progressive tissue damage. Studies over the past years focused on foods rich in polyphenols with anti-inflammatory and immunomodulatory properties, since inflammation was recognized to play a central role in several diseases. In this review, we discuss the beneficial effects of resveratrol, the most widely investigated polyphenol, on cancer and neurodegenerative, respiratory, metabolic, and cardiovascular diseases. We highlight how resveratrol, despite its unfavorable pharmacokinetics, can modulate the inflammatory pathways underlying those diseases, and we identify future opportunities for the evaluation of its clinical feasibility.

Analgesic and anti-inflammatory effects of resveratrol in rat models of pain: Any role in clinical pain management?

Background: Resveratrol (RSV) is a biomolecule that has been demonstrated in numerous studies to possess therapeutic potentials with multiple targets. Despite the reported low bioavailability, it could exhibit novel role in clinical pain management. Objective: To investigate the systemic analgesic and anti-inflammatory effects of RSV in comparison to diclofenac and etoricoxib. Materials and Methods: Following institutional ethics approval, the study was conducted in the physiology research laboratory. The animals (42 male Wistar rats) used were divided into seven groups (n = 6) in separate cages. Chemical pain was evaluated using formalin-induced nociception test. Statistical analysis was done using analysis of variance and Kruskal–Wallis statistical tests. Results: There is a significant change in nociceptive score in the early phase; however, no significant changes in the late phase in the formalin test. Anti-inflammatory studies showed that RSV 50 mg/kg has a significantly potent anti-inflammatory effect when compared to control, but similar in activity to etoricoxib. Tumor necrosis factor alpha and interleukin-2 concentration did not significantly differ between the groups. Conclusion: RSV may elicit its analgesic actions by inhibiting the direct activation of nociceptors. It may be suggested that systemic RSV at a dose of 50 mg/kg in Wistar rats significantly reduces inflammation comparable to etoricoxib, but possibly less potent than diclofenac. Thus, RSV may be useful in the management of acute and chronic pain with significant inflammatory components. Further broad based human clinical studies on the analgesic and anti-inflammatory properties of resveratrol are required to confirm its potential role in clinical pain management.

Resveratrol Ameliorates Palmitate-Induced Inflammation in Skeletal Muscle Cells by Attenuating Oxidative Stress and JNK/NF-κB Pathway in a SIRT1-Independent Mechanism.

Resveratrol has been shown to exert anti-inflammatory and anti-oxidant effects in a variety of cell types, however, its role in prevention of inflammatory responses mediated by palmitate in skeletal muscle cells remains unexplored. In the present study, we investigated the effects of resveratrol on palmitate-induced inflammation and elucidated the underlying mechanisms in skeletal muscle cells. The results showed that palmitate significantly enhanced TNF-α and IL-6 mRNA expression and protein secretion from C2C12 cells at 12, 24, and 36 h treatments. Increased expression of cytokines was accompanied by an enhanced phosphorylation of JNK, P38, ERK1/2, and IKKα/IKKβ. In addition, JNK and P38 inhibitors could significantly attenuate palmitate-induced mRNA expression of TNF-α and IL-6, respectively, whereas NF-κB inhibitor reduced the expression of both cytokines in palmitate-treated cells. Resveratrol pretreatment significantly prevented palmitate-induced TNF-α and IL-6 mRNA expression and protein secretion in C2C12 cells. Importantly, pre-treatment of the cells with resveratrol completely abrogated the phosphorylation of ERK1/2, JNK, and IKKα/IKKβ in palmitate treated cells. The protection from palmitate-induced inflammation by resveratrol was accompanied by a decrease in the generation of reactive oxygen species (ROS). N-acetyl cysteine (NAC), a known scavenger of ROS, could protect palmitate-induced expression of TNF-α and IL-6. Furthermore, inhibition of SIRT1 by shRNA or sirtinol demonstrated that the anti-inflammatory effect of resveratrol in muscle cells is mediated through a SIRT1-independent mechanism. Taken together, these findings suggest that resveratrol may represent a promising therapy for prevention of inflammation in skeletal muscle cells. J. Cell. Biochem. 118: 2654-2663, 2017. © 2017 Wiley Periodicals, Inc.

Resveratrol relieves Angiostrongylus cantonensis – Induced meningoencephalitis by activating sirtuin-1

Resveratrol, a natural herbal compound found in high levels in grapes and red wine, is frequently used as activator of sirtuin-1. This study investigated the potential function of sirtuin-1 in regulating angiostrongyliasis meningoencephalitis in resveratrol-treated mice. Mice were subjected to meningoencephalitis to study the protective effect of resveratrol against meningoencephalitis and investigate the effects of sirtuin-1 activation on brain. Results demonstrated that sirtuin-1 level decreased in mice with meningoencephalitis and significantly increased in resveratrol-treated mice. Moreover, resveratrol treatment significantly reduced eosinophil counts, p65, Interferon-γ, interleukin (IL)-5, IL-33, and tumor necrosis factor-α levels, matrix metalloproteinase-9 activity, claudin-5 degradation, and blood–brain barrier permeability. By contrast, the anti-inflammatory factor IL-10 was significantly increased in resveratrol-treated mice. Resveratrol treatment was partially beneficial in controlling the pathological processes of angiostrongyliasis meningoencephalitis. The results demonstrate the neuroprotective and anti-inflammatory effects of resveratrol against Angiostrongylus cantonensis-induced eosinophilic meningoencephalitis in mice. Treatment with sirtuin-1 agonist was given within a therapeutic window after A. cantonensis infection.

Resveratrol inhibits LPS-induced mice mastitis through attenuating the MAPK and NF-κB signaling pathway.

Resveratrol is a natural polyphenol extracted from mangy plants. It has been reported that resveratrol show multitudinous positive role in biology such as anti-oxidant, anti-nociception and anti-inflammatory effects. Therefore, the present study devotes to test the effect of resveratrol on LPS-induced mastitis in mice. Resveratrol was administered intraperitoneally 1h before LPS treatment. And the anti-inflammatory effect of resveratrol was measured by histopathological examination, MPO assay, real-time PCR and western blotting analysis. The results showed that resveratrol significantly reduced the LPS-induced mammary histopathological changes. Meanwhile, it sharply attenuated the activity of MPO. The result also indicated that the resveratrol can decrease the expression of pro-inflammatory cytokines TNF-α and IL-1β. From the results of western blotting, resveratrol suppressed the expression of phosphorylation of p65 and IκB from NF-κB signal pathway and phosphorylation of p38 and ERK from MAPK signal pathway. These findings suggested that resveratrol may inhibit the inflammatory response in the mastitis.

Anti-inflammatory effect of resveratrol in human coronary arterial endothelial cells via induction of autophagy: implication for the treatment of Kawasaki disease

BackgroundKawasaki disease (KD) is an acute febrile vasculitis in childhood, which is the leading cause of acquired heart disease in children. If untreated, KD can result in coronary aneurysms in 25% of patients, and even under intravenous immunoglobulin (IVIG) treatment, 10–20% of children will have IVIG resistance and increased risk of developing coronary arteritis complication. Additional therapies should be explored to decrease the incidence of coronary artery lesions and improve the prognosis in KD. Autophagy has been reported to play a critical role in a variety of heart diseases. Resveratrol (RSV) confers cardio protection during ischemia and reperfusion in rats via activation of autophagy. Serum TNF-alpha levels are elevated in KD, which might activate the endothelial cells to express intercellular adhesion molecule-1 (ICAM-1), vascular cellular adhesion molecule-1(VCAM-1), inducible nitric oxide synthase (iNOS) and IL-1β.MethodsHuman coronary arterial endothelial cells (HCAECs) were either untreated or treated by TNF-α 10 ng/ml for 2 h in the presence or absence of RSV or autophagy-related protein 16-like 1 (Atg16L1) siRNA. Total RNA was analyzed by real-time quantitative PCR for ICAM-1, VCAM-1, iNOS and IL-1β mRNA expressions. The involvement of autophagy proteins was investigated by Western blot.ResultsPretreatment with resveratrol significantly inhibited TNF-α-induced ICAM-1, iNOS and IL-1β mRNA expression in HCAECs. Western blot revealed the enhanced autophagy proteins LC3B and Atg16L1 expression by RSV. The suppressive effects of RSV were obviously counteracted by Atg16L1 siRNA.ConclusionsWe demonstrated RSV had anti-inflammatory effects on HCAECs via induction of autophagy. Our results suggest that resveratrol may modulate the inflammatory response of coronary artery in KD and explore the role of autophagy in the pathogenesis and alternative therapy of coronary arterial lesions in KD.

Anti-inflammatory Effects of Resveratrol on Hypoxia/Reoxygenation-Induced Alveolar Epithelial Cell Dysfunction.

Reducing oxidative stress is crucial to prevent hypoxia-reoxygenation (H/R)-induced lung injury. Resveratrol has excellent antioxidant and anti-inflammatory effects, and this study investigated its role in H/R-induced type II pneumocyte dysfunction. H/R conditions increased expression of inflammatory cytokines including interleukin (IL)-1β (142.3 ± 21.2%, P < 0.05) and IL-6 (301.9 ± 35.1%, P < 0.01) in a type II alveolar epithelial cell line (A549), while the anti-inflammatory cytokine IL-10 (64.6 ± 9.8%, P < 0.05) and surfactant proteins (SPs) decreased. However, resveratrol treatment effectively inhibited these effects. H/R significantly activated an inflammatory transcription factor, nuclear factor (NF)-κB, while resveratrol significantly inhibited H/R-induced NF-κB transcription activities. To the best of our knowledge, this is the first study showing resveratrol-mediated reversal of H/R-induced inflammatory responses and dysfunction of type II pneumocyte cells in vitro. The effects of resveratrol were partially mediated by promoting SP expression and inhibiting inflammation with NF-κB pathway involvement. Therefore, our study provides new insights into mechanisms underlying the action of resveratrol in type II pneumocyte dysfunction.

Anti-Inflammatory Effects of Resveratrol in Patients with Ulcerative Colitis: A Randomized, Double-Blind, Placebo-controlled Pilot Study

Ulcerative colitis (UC) is a chronic idiopathic inflammatory disease in which reducing pro-inflammatory and/or increasing anti-inflammatory molecules is the mainstay of treatment. The aim of this study was to evaluate the effects of supplementation with resveratrol as an antiinflammatory and antioxidant agent on inflammation and quality of life in patients with active UC. In this randomized, double-blind, placebo-controlled study, 50 eligible patients with active mild to moderate UC were supplemented with either a 500-mg resveratrol or placebo capsule for 6 weeks. Serum inflammatory markers, activity of NF-κB in peripheral blood mononuclear cells (PBMC) and quality of life were assessed at baseline and at the end of the study. Resveratrol supplementation led to a significant reduction in plasma levels of TNF-α (19.70 ± 12.80 to 17.20 ± 10.09 pg/mL) and hs-CRP (4764.25 ± 2260.48 to 2584.50 ± 1792.80 ng/mL) and activity of NF-κB in PBMCs (0.19 ± 0.05 to 0.10 ± 0.04 OD) (p <0.001), whereas there were no significant changes of these factors in placebo group. Also, the score of inflammatory bowel disease questionnaire -9 (IBDQ-9) increased, whereas the clinical colitis activity index score decreased significantly in the resveratrol group (32.72 ± 7.52 to 47.64 ± 8.59) (p <0.001) and when compared with the placebo group (35.54 ± 9.50 to 41.08 ± 6.59) (p <0.001). Our results indicate that 6 weeks supplementation with 500 mg resveratrol can improve quality of life and disease clinical colitis activity at least partially through inflammation reduction in patients with UC. Whether these effects will be continued in longer duration of treatment remains to be determined.