Anti-Inflammatory evaluation of black rice extract inhibits TNF-α, IFN-γ and IL-6 cytokines produced by immunocompetent cells
TL;DR: In this paper, the anti-inflammatory activity of ethanol extract and aqueous extract of black rice was compared in vitro on splenocytes of diabetes mellitus mice model as the control of inflammation Cells were cultured in Roswell Park Memorial Institute medium with 10% fetal bovine serum, anti-CD3 and lipopolysaccharide and black rice extract 50, 100 and 200
Abstract: Black rice has been known for its many beneficial effects to our body because it contains several chemical compounds that act as anti-inflammatory agents This study aims to compare the anti-inflammatory activity of ethanol extract and aqueous extract of black rice Anti-inflammatory activity test was performed in vitro on splenocytes of diabetes mellitus mice model as the control of inflammation Cells were cultured in Roswell Park Memorial Institute medium with 10% fetal bovine serum, anti-CD3 and lipopolysaccharide and black rice extract 50, 100 and 200 µg/mL In day 3, cells were harvested, stained and analyzed by flow cytometry The result shows that the ethanol extract and aqueous extract of black rice have anti-inflammatory activity 50 µg/mL black rice aqueous extract has the most extensive anti-inflammatory activity indicated by increased Treg cells, decreased nuclear factor kappa B activity on CD4+, CD8+ T cells, decreased production of TNF-α by CD4+ T cells, decreased production of IL-6
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TL;DR: YGIYPR as mentioned in this paper was identified as Tyr-Gly-Ile-Tyr-Pro-Arg by high-performance liquid chromatography electrospray ionization quadrupole time-of-flight mass spectrometer.
Abstract: To prepare immunomodulation peptides from rice protein hydrolysates (RPHs), trypsin was employed for enzymatic hydrolysis, and the immunomodulating activities of RPHs were studied using mouse peritoneal macrophage proliferation assay. The peptide fractions with the highest activity were further purified using macroporous adsorption resin, strong cation-exchange chromatography, gel filtration chromatography and reversed-phase high-performance liquid chromatography. The peptide sequence was identified as Tyr-Gly-Ile-Tyr-Pro-Arg (YGIYPR) by high-performance liquid chromatography electrospray ionization quadrupole time-of-flight mass spectrometer. Evaluating its immunomodulatory activity showed that YGIYPR enhanced the proliferation of macrophage RAW 264.7 cells in the range of 12.5–100 μg/mL, and even a minimum dose achieved good proliferation. The results demonstrated that the RPHs prepared by trypsin could serve as a source of immunomodulating peptides and the immunomodulatory peptide YGIYPR is a p...
13 citations
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TL;DR: CTAB-modified PSP-Cubs/OVA could promote the secretion of related cytokines and the proliferation of lymphocytes, stimulate the cellular immune response and increase the level of humoral immunity.
Abstract: Recently, the cubosomes have been widely studied as drug carriers. It has been described that cubosomes could further stimulate the immune response after carrying the immune enhancer. Polygonatum sibiricum polysaccharide (PSP), one of the most important biologically active ingredients of Polygonatum sibiricum, has been reported as an immunostimulant to improve immune responses. This study was aimed to observe the immunomodulation effects of ovalbumin (OVA) absorbed cetyltrimethylammonium bromide-modified Polygonatum sibiricum polysaccharide cubosomes (CTAB-modified PSP-Cubs/OVA). Firstly, the antigen uptake of CTAB-modified PSP-Cubs/OVA by macrophages was determined in vitro. After that, mice were immunized with CTAB-modified PSP-Cubs/OVA. The activation of dendritic cells in lymph nodes, activation of lymphocyte, ratios of CD4+ to CD8+, the concentrations of OVA-specific IgG in serum and the cytokines concentrations were analyzed. As the results showed, CTAB-modified PSP-Cubs/OVA could promote the production of OVA-specific IgG in serum. The ratio of CD4+ to CD8+ in CTAB-modified PSP-Cubs/OVA group was significantly increased compared with other groups. CTAB-modified PSP-Cubs/OVA could significantly activate dendritic cells and promote lymphocyte proliferation. The results indicated that CTAB-modified PSP-Cubs/OVA could promote the secretion of related cytokines and the proliferation of lymphocytes, stimulate the cellular immune response and increase the level of humoral immunity. Above all, CTAB-modified PSP-Cubs had good adjuvant activity.
11 citations
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TL;DR: In this article, the effects of derivatives from Euterpe spp. fruits on oxidative metabolism and inflammatory mediators were evaluated, and the results indicated that dietary supplementation with extracts of E.edulis has no deleterious effects and may be beneficial, especially for LEDE extracts containing high concentrations of anthocyanin.
Abstract: Fruits of Euterpe spp. are rich in phenolic compounds, mainly anthocyanins, which are endowed with a high antioxidant capacity. The objective of the study was to evaluate the effects of derivatives from Euterpe spp. fruits on oxidative metabolism and inflammatory mediators. The oil (OE), total lyophilized pulp (LEE) and defatted pulp (LEDE) were obtained from the fruits of Euterpe edulis. Thirty-six animals were divided into four experimental groups: G1: Control; G2: OE (4%), G3: LEE (10%), G4: LEDE (10%), each of which received a particular extract in their diet for 50 days. The activities of catalase, glutathione-S-transferase, superoxide dismutase, malondialdehyde produced in liver and expression of pro-inflammatory cytokines tissue were lower in G4 than in the other groups. The study indicates that dietary supplementation with extracts of E. edulis has no deleterious effects and may be beneficial, especially for LEDE extracts containing high concentrations of anthocyanin.
8 citations
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TL;DR: The effects of various intake levels of soybean oil on carbohydrate metabolism and inflammation in mice were studied in this article, where the optimal intake of soybeans was found to lead to excessive weight gain, higher levels of fasting blood glucose and serum insulin, increased levels of tumor necrosis factor-α, interleukin 6, hyper-sensitive C-reactive protein, and reduced expression of IRS1 and IRS2 mRNA.
Abstract: The effects of various intake levels of soybean oil on carbohydrate metabolism and inflammation in mice were studied. Mice were supplied with different diets, in which soybean oil provided 5, 10, 15, 20, 25, and 30% of total energy. Blood glucose indices, blood fat indices, inflammatory factors, and gene expression of insulin receptor substrates 1 and 2 Insulin receptor substrate 1 (IRS1) and Insulin receptor substrate 2 (IRS2) were analyzed. The results showed that higher intake of soybean oil can lead to excessive weight gain, higher levels of fasting blood glucose and serum insulin, increased levels of tumor necrosis factor-α, interleukin 6, hyper-sensitive C-reactive protein, and reduced expression of IRS1 and IRS2 mRNA. Primarily, we found that reduced intake of soybean oil led to a similar trend to that of a high soybean oil diet. The optimal intake of soybean oil, as supplied in the diet, was about 15–20%.
5 citations
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TL;DR: It is suggested that WEPA can inhibit the growth of mouse 4T1 tumours through modulating immune system of the mouse.
Abstract: Pilose antler (PA) is used to treat many diseases, but its effect on breast cancer is still unclear. Here, we report the effects of PA on the growth of the mouse mammary tumour in vitro and in vivo...
3 citations
References
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TL;DR: How genetic evidence in mice has revealed complex roles for the NF-kappaB in inflammation that suggest both pro- and anti-inflammatory roles for this pathway is described.
Abstract: The nuclear factor NF-κB pathway has long been considered a prototypical proinflammatory signaling pathway, largely based on the role of NF-κB in the expression of proinflammatory genes including cytokines, chemokines, and adhesion molecules In this article, we describe how genetic evidence in mice has revealed complex roles for the NF-κB in inflammation that suggest both pro- and anti-inflammatory roles for this pathway NF-κB has long been considered the “holy grail” as a target for new anti-inflammatory drugs; however, these recent studies suggest this pathway may prove a difficult target in the treatment of chronic disease In this article, we discuss the role of NF-κB in inflammation in light of these recent studies
2,545 citations
"Anti-Inflammatory evaluation of bla..." refers background in this paper
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TL;DR: This study shows that in these models, IL-23 is essential for manifestation of chronic intestinal inflammation, whereas IL-12 is not, and a critical target of IL- 23 is a unique subset of tissue-homing memory T cells, which are specifically activated by IL-21 to produce the proinflammatory mediators IL-17 and IL-6.
Abstract: Uncontrolled mucosal immunity in the gastrointestinal tract of humans results in chronic inflammatory bowel disease (IBD), such as Crohn disease and ulcerative colitis. In early clinical trials as well as in animal models, IL-12 has been implicated as a major mediator of these diseases based on the ability of anti-p40 mAb treatment to reverse intestinal inflammation. The cytokine IL-23 shares the same p40 subunit with IL-12, and the anti-p40 mAbs used in human and mouse IBD studies neutralized the activities of both IL-12 and IL-23. IL-10-deficient mice spontaneously develop enterocolitis. To determine how IL-23 contributes to intestinal inflammation, we studied the disease susceptibility in the absence of either IL-23 or IL-12 in this model, as well as the ability of recombinant IL-23 to exacerbate IBD induced by T cell transfer. Our study shows that in these models, IL-23 is essential for manifestation of chronic intestinal inflammation, whereas IL-12 is not. A critical target of IL-23 is a unique subset of tissue-homing memory T cells, which are specifically activated by IL-23 to produce the proinflammatory mediators IL-17 and IL-6. This pathway may be responsible for chronic intestinal inflammation as well as other chronic autoimmune inflammatory diseases.
1,476 citations
"Anti-Inflammatory evaluation of bla..." refers background in this paper
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TL;DR: The critical link between inflammation and cancer is described and observations imply that anti-inflammatory agents that suppress NF-kappaB or NF- kappaB-regulated products should have a potential in both the prevention and treatment of cancer.
Abstract: Although inflammation has long been known as a localized protective reaction of tissue to irritation, injury, or infection, characterized by pain, redness, swelling, and sometimes loss of function, there has been a new realization about its role in a wide variety of diseases, including cancer. While acute inflammation is a part of the defense response, chronic inflammation can lead to cancer, diabetes, cardiovascular, pulmonary, and neurological diseases. Several pro-inflammatory gene products have been identified that mediate a critical role in suppression of apoptosis, proliferation, angiogenesis, invasion, and metastasis. Among these gene products are TNF and members of its superfamily, IL-1alpha, IL-1beta, IL-6, IL-8, IL-18, chemokines, MMP-9, VEGF, COX-2, and 5-LOX. The expression of all these genes are mainly regulated by the transcription factor NF-kappaB, which is constitutively active in most tumors and is induced by carcinogens (such as cigarette smoke), tumor promoters, carcinogenic viral proteins (HIV-tat, HIV-nef, HIV-vpr, KHSV, EBV-LMP1, HTLV1-tax, HPV, HCV, and HBV), chemotherapeutic agents, and gamma-irradiation. These observations imply that anti-inflammatory agents that suppress NF-kappaB or NF-kappaB-regulated products should have a potential in both the prevention and treatment of cancer. The current review describes in detail the critical link between inflammation and cancer.
1,215 citations
Journal Article•
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TL;DR: Th1/Th2-based immunotherapies, e.g., T-cell receptor peptides and interleukin-4 (IL-4) injections, have produced mixed results to date and many diseases previously classified as Th1 or Th2 dominant fail to meet the set criteria.
Abstract: One theory of immune regulation involves homeostasis between T-helper 1 (Th1) and Thelper 2 (Th2) activity. The Th1/Th2 hypothesis arose from 1986 research suggesting mouse T-helper cells expressed differing cytokine patterns. This hypothesis was adapted to human immunity, with Th1- and Th2-helper cells directing different immune response pathways. Th1 cells drive the type-1 pathway (“cellular immunity”) to fight viruses and other intracellular pathogens, eliminate cancerous cells, and stimulate delayed-type hypersensitivity (DTH) skin reactions. Th2 cells drive the type-2 pathway (“humoral immunity”) and up-regulate antibody production to fight extracellular organisms; type 2 dominance is credited with tolerance of xenografts and of the fetus during pregnancy. Overactivation of either pattern can cause disease, and either pathway can down-regulate the other. But the hypothesis has major inconsistencies; human cytokine activities rarely fall into exclusive proTh1 or -Th2 patterns. The non-helper regulatory T cells, or the antigen-presenting cells (APC), likely influence immunity in a manner comparable to Th1 and Th2 cells. Many diseases previously classified as Th1 or Th2 dominant fail to meet the set criteria. Experimentally, Th1 polarization is readily transformed to Th2 dominance through depletion of intracellular glutathione, and vice versa. Mercury depletes glutathione and polarizes toward Th2 dominance. Several nutrients and hormones measurably influence Th1/Th2 balance, including plant sterols/ sterolins, melatonin, probiotics, progesterone, and the minerals selenium and zinc. The longchain omega-3 fatty acids EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) significantly benefit diverse inflammatory and autoimmune conditions without any specific Th1/Th2 effect. Th1/Th2-based immunotherapies, e.g., T-cell receptor (TCR) peptides and interleukin-4 (IL4) injections, have produced mixed results to date. (Altern Med Rev 2003;8(3):223-246)
959 citations
"Anti-Inflammatory evaluation of bla..." refers background in this paper
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TL;DR: This work proposes that there may be a key suppressive mechanism that is shared by every forkhead box p3 (Foxp3)(+) Treg in vivo and in vitro in mice and humans and will help to design effective ways for controlling immune responses by targeting Treg suppressive functions.
Abstract: Regulatory T cells (Tregs), either natural or induced, suppress a variety of physiological and pathological immune responses. One of the key issues for understanding Treg function is to determine how they suppress other lymphocytes at the molecular level in vivo and in vitro. Here we propose that there may be a key suppressive mechanism that is shared by every forkhead box p3 (Foxp3) 1 Treg in vivo and in vitro in mice and humans. When this central mechanism is abrogated, it causes a breach in self-tolerance and immune homeostasis. Other suppressive mechanisms may synergistically operate with this common mechanism depending on the environment and the type of an immune response. Further, Treg-mediated suppression is a multi-step process and impairment or augmentation of each step can alter the ultimate effectiveness of Treg-mediated suppression. These findings will help to design effective ways for controlling immune responses by targeting Treg suppressive functions.
769 citations
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