Displaying publications 1 - 20 of 64 in total

  1. Sharma JN, Buchanan WW
    Exp. Toxicol. Pathol., 1994 Dec;46(6):421-33.
    PMID: 7703672 DOI: 10.1016/S0940-2993(11)80053-9
    Excessive release of kinin (BK) in the synovial fluid can produce oedema, pain and loss of functions due to activation of B1 and B2 kinin receptors. Activation of the kinin forming system could be mediated via injury, trauma, coagulation pathways (Hageman factor and thrombin) and immune complexes. The activated B1 and B2 receptors might cause release of other powerful non-cytokine and cytokine mediators of inflammation, e.g., PGE2, PGI2, LTs, histamine, PAF, IL-1 and TNF, derived mainly from polymorphonuclear leukocytes, macrophages, endothelial cells and synovial tissue. These mediators are capable of inducing bone and cartilage damage, hypertrophic synovitis, vessel proliferation, inflammatory cell migration and, possibly, angiogenesis in pannus formation. These pathological changes, however, are not yet defined in the human model of chronic inflammation. The role of kinins and their interacting inflammatory mediators would soon start to clarify the detailed questions they revealed in clinical and experimental models of chronic inflammatory diseases. Several B1 and B2 receptor antagonists are being synthesized in an attempt to study the molecular functions of kinins in inflammatory processes, such as rheumatoid arthritis, periodontitis, inflammatory diseases of the gut and osteomyelitis. Future development of specific potent and stable B1 and B2 receptor antagonists or combined B1 and B2 antagonists with y-IFN might serve as a pharmacological basis for more effective treatment of joint inflammatory and related diseases.
    Matched MeSH terms: Inflammation Mediators/metabolism
  2. Leong XF, Ng CY, Badiah B, Das S
    ScientificWorldJournal, 2014;2014:768237.
    PMID: 24526921 DOI: 10.1155/2014/768237
    This review is to examine the current literatures on the relationship between periodontitis and hypertension as well as to explore the possible biological pathways underlying the linkage between these health conditions. Hypertension is one of the major risk factors for cardiovascular diseases. Oxidative stress and endothelial dysfunction are among the critical components in the development of hypertension. Inflammation has received much attention recently and may contribute to a pivotal role in hypertension. Periodontitis, a chronic low-grade inflammation of gingival tissue, has been linked to endothelial dysfunction, with blood pressure elevation and increased mortality risk in hypertensive patients. Inflammatory biomarkers are increased in hypertensive patients with periodontitis. Over the years, various researches have been performed to evaluate the involvement of periodontitis in the initiation and progression of hypertension. Many cross-sectional studies documented an association between hypertension and periodontitis. However, more well-designed prospective population trials need to be carried out to ascertain the role of periodontitis in hypertension.
    Matched MeSH terms: Inflammation Mediators/metabolism*
  3. Sejari N, Kamaruddin K, Ramasamy K, Lim SM, Neoh CF, Ming LC
    BMC Complement Altern Med, 2016 Jan 15;16:16.
    PMID: 26767971 DOI: 10.1186/s12906-016-0988-1
    BACKGROUND: The treatment of low back pain is very challenging due to the recurrent nature of the problem. It is believed that traditional Malay massage helps to relieve such back pain but there is a lack of scientific evidence to support both the practice of traditional Malay massage and the mechanism by which it exerts its effect. The aim of this study is to investigate the immediate effect of traditional Malay massage on the pain scale, substance P, inflammatory mediators, and functional outcomes among low back pain patients.

    METHODS: A non-blinded, randomised controlled trial will be conducted. A total of sixty-six patients who fulfil the inclusion criteria will be recruited. The participants will be randomly allocated into intervention (traditional Malay massage) and control (relaxation position) groups. Blood and saliva samples will be collected before and immediately after intervention. All collected samples will be analysed. The primary outcomes are the changes in the level of substance P in both saliva and blood samples between both groups. The secondary outcomes include the levels of inflammatory mediators [i.e. TNF-α, IL-1β, IL-8, monocyte chemotactic protein-1, IL-6 and IL-10, and the soluble form of the intercellular adhesion molecule], the pain intensity as measured by a visual analogous scale and functional outcomes using the Roland-Morris Disability Questionnaire.

    DISCUSSION: Massage is a type of physical therapy that has been proven to be potentially capable of reducing unpleasant pain sensations by a complex sensory response and chemical mediators such as substance P and various inflammatory mediators. Previous studies conducted using Thai, Swedish, or other forms of massage therapies, have showed inconsistent findings on substance P levels pre and post the interventions. Each massage genre varies in terms of massage and joint mobilization points, as well as the lumbar spinous process. Traditional Malay massage, known locally as "Urut Melayu", involves soft-tissue manipulation of the whole body applied using the hands and fingers. This massage technique combines both deep muscular tissue massage and spiritual rituals. This trial is expected to give rise to new knowledge underlying the mechanisms for pain and inflammation relief that are activated by traditional Malay massage.

    TRIAL REGISTRATION: Australian New Zealand Clinical Trials ACTRN12615000537550 .

    Matched MeSH terms: Inflammation Mediators/metabolism*
  4. Sharma JN
    Eur J Rheumatol Inflamm, 1991;11(2):30-7.
    PMID: 1365470
    Components of the kallikrein-kininogen-kinin are activated in response to noxious stimuli (chemical, physical or bacterial), which may lead to excessive release of kinins in the synovial joints that may produce inflammatory joint disease. The inflammatory changes observed in synovial tissue may be due to activation of B2 receptors. Kinins also stimulate the synthesis of other pro-inflammatory agents (PGs, LTs, histamine, EDRF, PGI2 and PAF) in the inflamed joint. B2 receptor antagonists may provide valuable agents as new analgesic drugs. Further, it is suggested that substances directed to reduce the activation of KKS may provide a pharmacological basis for the synthesis of novel anti-rheumatic or anti-inflammatory drugs.
    Matched MeSH terms: Inflammation Mediators/metabolism
  5. A/L B Vasanth Rao VR, Tan SH, Candasamy M, Bhattamisra SK
    Diabetes Metab Syndr, 2018 11 30;13(1):754-762.
    PMID: 30641802 DOI: 10.1016/j.dsx.2018.11.054
    Diabetic nephropathy (DN) is a major cause of end-stage renal disease and affects a large number of individuals with diabetes. However, the development of specific treatments for DN has not yet been identified. Hence, this review is concisely designed to understand the molecular pathways leading to DN in order to develop suitable therapeutic strategies. Extensive literature search have been carried in regard with the pathogenesis and pathophysiology of DN, drug targets and updates on clinical trials, the consequences associated with DN and the potential biomarkers for diagnosis and prediction of DN are discussed in this review. DN is characterised by microalbuminuria and macroalbuminuria, and morphological changes such as glomerular thickening, interstitial fibrosis, formation of nodular glomerulosclerosis and decreased endothelial cell fenestration. Besides, the involvement of renin-angiotensin-aldosterone system, inflammation and genetic factors are the key pathways in the progression of DN. In regard with drug development drugs targeted to epidermal growth factor, inflammatory cytokines, ACTH receptor and TGFβ1 receptors are in pipeline for clinical trials whereas, several drugs have also failed in phase III and phase IV of clinical trials due to lack of efficacy and severe adverse effect. The research on DN is limited with respect to its pathogenesis and drug development. Thus, a more detailed understanding of the pathogenesis of DN is very essential to progress in the drug development process.
    Matched MeSH terms: Inflammation Mediators/metabolism
  6. Zakaria R, Wan Yaacob WM, Othman Z, Long I, Ahmad AH, Al-Rahbi B
    Physiol Res, 2017 09 22;66(4):553-565.
    PMID: 28406691
    Alzheimer's disease (AD) is a primary cause of dementia in the middle-aged and elderly worldwide. Animal models for AD are widely used to study the disease mechanisms as well as to test potential therapeutic agents for disease modification. Among the non-genetically manipulated neuroinflammation models for AD, lipopolysaccharide (LPS)-induced animal model is commonly used. This review paper aims to discuss the possible factors that influence rats' response following LPS injection. Factors such as dose of LPS, route of administration, nature and duration of exposure as well as age and gender of animal used should be taken into account when designing a study using LPS-induced memory impairment as model for AD.
    Matched MeSH terms: Inflammation Mediators/metabolism
  7. Kow ASF, Chik A, Soo KM, Khoo LW, Abas F, Tham CL
    Front Immunol, 2019;10:190.
    PMID: 30809224 DOI: 10.3389/fimmu.2019.00190
    Background: Anaphylaxis is an acute and life-threatening allergic response. Classically and most commonly, it can be mediated by the crosslinking of allergens to immunoglobulin E (IgE)- high affinity IgE receptor (FcεRI) complex found mostly on mast cells. However, there is another pathway of anaphylaxis that is less well-studied. This pathway known as the alternative pathway is mediated by IgG and its Fc gamma receptor (Fcγ). Though it was not documented in human anaphylaxis, a few studies have found that IgG-mediated anaphylaxis can happen as demonstrated in rodent models of anaphylaxis. In these studies, a variety of soluble mediators were being evaluated and they differ from each study which causes confusion in the suitability, and reliability of choice of soluble mediators to be analyzed for diagnosis or therapeutic purposes. Hence, the objective of this meta-analysis is to identify the potential soluble mediators that are involved in an IgG-mediated anaphylaxis reaction. Methods: Studies related to IgG-mediated anaphylaxis were sourced from five search engines namely PubMed, Scopus, Ovid, Cochrane Library, and Center for Agricultural Bioscience International (CABI) regardless of publication year. Relevant studies were then reviewed based on specific inclusion factors. The means and standard deviations of each soluble mediator studied were then extracted using ImageJ or Get Data Graph Digitiser software and the data were subjected to meta-analysis. Results: From our findings, we found that histamine, serotonin, platelet activating factor (PAF), β-hexosaminidase, leukotriene C4 (LTC4), mucosal mast cell protease-1 (MMCP-1), interleukins (IL)-4,-6, and-13; tumor necrosis factor alpha (TNF-α), and macrophage inflammatory protein-1α (MIP-1α) were often being analyzed. Out of these soluble mediators, histamine, PAF, β-hexosaminidase, IL-6, and-13, MIP-1α and TNF-α were more significant with positive effect size and p < 0.001. As study effect was relatively small, we performed publication bias and found that there was publication bias and this could be due to the small sample size studied. Conclusion: As such, we proposed that through meta-analysis, the potential soluble mediators involved in rodent IgG-mediated anaphylaxis to be histamine, PAF, β-hexosaminidase, IL-6 and-13 and MIP-1α, and TNF-α but will require further studies with larger sample size.
    Matched MeSH terms: Inflammation Mediators/metabolism
  8. Ooi TC, Ahmad A, Rajab NF, Sharif R
    Nutrients, 2023 Jul 18;15(14).
    PMID: 37513601 DOI: 10.3390/nu15143184
    Senescence is a normal biological process that is accompanied with a series of deteriorations in physiological function. This study aimed to investigate the effects of bovine colostrum milk supplementation on metabolic changes and the expression of various biomarkers on inflammation, antioxidant and oxidative damage, nutrient metabolism, and genomic stability among older adults. Older adults (50-69 years old) who participated in the 12-week randomized, double-blinded, placebo-controlled trial were instructed to consume the IgCo bovine colostrum-enriched skim milk or regular skim milk (placebo) twice daily. Following 12 weeks of intervention, participants in the intervention group had lower expression levels in pro-inflammatory mediators (CRP, IL-6, and TNF-α), with significant (p < 0.05) interaction effects of the group and time observed. However, no significant interaction effect was observed in the vitamin D, telomerase, 8-OHdG, MDA, and SOD activities. UPLC-MS-based untargeted metabolomics analysis revealed that 22 metabolites were upregulated and 11 were downregulated in the intervention group compared to the placebo group. Glycerophospholipid metabolism, along with cysteine and methionine metabolism were identified as the potential metabolic pathways that are associated with bovine colostrum milk consumption. In conclusion, consuming bovine colostrum milk may induce metabolic changes and reduce the expression of various pro-inflammatory mediators, thus improving the immune function in older adults.
    Matched MeSH terms: Inflammation Mediators/metabolism
  9. Kharitonova M, Iezhitsa I, Zheltova A, Ozerov A, Spasov A, Skalny A
    J Trace Elem Med Biol, 2015 Jan;29:227-34.
    PMID: 25127069 DOI: 10.1016/j.jtemb.2014.06.026
    Magnesium (Mg) deficiency is implicated in the development of numerous disorders of the cardiovascular system. Moreover, the data regarding the efficacy of different magnesium compounds in the correction of impaired functions due to low magnesium intake are often fragmentary and inconsistent. The aim of this study was to compare the effects of the most bioavailable Mg compounds (Mg l-aspartate, Mg N-acetyltaurate, Mg chloride, Mg sulphate and Mg oxybutyrate) on systemic inflammation and endothelial dysfunction in rats fed a low Mg diet for 74 days. A low Mg diet decreased the Mg concentration in the plasma and erythrocytes, which was accompanied by a reduced concentration of eNOs and increased levels of endothelin-1 level in the serum and impaired endothelium-dependent vasodilatation. These effects increased the concentration of proinflammatory molecules, such as VCAM-1, TNF-α, IL-6 and CRP, indicating the development of systemic inflammation and endothelial dysfunction. The increased total NO level, which estimated from the sum of the nitrate and nitrite concentrations in the serum, may also be considered to be a proinflammatory marker. Two weeks of Mg supplementation partially or fully normalised the ability of the vascular wall to effect adequate endothelium-dependent vasodilatation and reversed the levels of most endothelial dysfunction and inflammatory markers (except CRP) to the mean values of the control group. Mg sulphate had the smallest effect on the endothelin-1, TNF-α and VCAM-1 levels. Mg N-acetyltaurate was significantly more effective in restoring the level of eNOS compared to all other studied compounds, except for Mg oxybutyrate. Taken together, the present findings demonstrate that all Mg compounds equally alleviate endothelial dysfunction and inflammation caused by Mg deficiency. Mg sulphate tended to be the least effective compound.
    Matched MeSH terms: Inflammation Mediators/metabolism
  10. Salim E, Kumolosasi E, Jantan I
    J Nat Med, 2014 Jul;68(3):647-53.
    PMID: 24799081 DOI: 10.1007/s11418-014-0841-0
    The inhibitory activities of the methanol extracts from 20 selected medicinal plants on the release of pro-inflammatory cytokines in human peripheral blood mononuclear cells (PBMCs) were evaluated. The major compound from the most active plant extract was also investigated. The inhibitory effect of the methanol extracts on the release of pro-inflammatory cytokines was tested by incubating PBMCs with the sample and then stimulating by lipopolysaccharide at 0.1 μg/ml. The level of cytokines was determined using enzyme-linked immunosorbent assay. Among the extracts tested, Andrographis paniculata extract demonstrated the strongest inhibition of interleukin (IL)-1β, IL-1α, and IL-6 release, with IC50 values of 1.54, 1.06, and 0.74 μg/ml, respectively. The IC50 value of A. paniculata extract was significantly higher than that of andrographolide on IL-1α, IL-1β, and IL-6 (p 
    Matched MeSH terms: Inflammation Mediators/metabolism
  11. Simarmata D, Ng DC, Kam YW, Lee B, Sum MS, Her Z, et al.
    Sci Rep, 2016 05 16;6:26097.
    PMID: 27180811 DOI: 10.1038/srep26097
    Chikungunya fever (CHIKF) is a global infectious disease which can affect a wide range of age groups. The pathological and immunological response upon Chikungunya virus (CHIKV) infection have been reported over the last few years. However, the clinical profile and immune response upon CHIKV infection in children remain largely unknown. In this study, we analyzed the clinical and immunological response, focusing on the cytokine/chemokine profile in a CHIKV-infected pediatric cohort from Sarawak, Malaysia. Unique immune mediators triggered upon CHIKV infection were identified through meta-analysis of the immune signatures between this pediatric group and cohorts from previous outbreaks. The data generated from this study revealed that a broad spectrum of cytokines/chemokines is up-regulated in a sub-group of virus-infected children stratified according to their viremic status during hospitalization. Furthermore, different immune mediator profiles (the levels of pro-inflammatory cytokines, chemokines and growth and other factors) were observed between children and adults. This study gives an important insight to understand the immune response of CHIKV infection in children and would aid in the development of better prognostics and clinical management for children.
    Matched MeSH terms: Inflammation Mediators/metabolism
  12. Sweeney S, Leo BF, Chen S, Abraham-Thomas N, Thorley AJ, Gow A, et al.
    Colloids Surf B Biointerfaces, 2016 Sep 01;145:167-75.
    PMID: 27182651 DOI: 10.1016/j.colsurfb.2016.04.040
    Accompanying increased commercial applications and production of silver nanomaterials is an increased probability of human exposure, with inhalation a key route. Nanomaterials that deposit in the pulmonary alveolar region following inhalation will interact firstly with pulmonary surfactant before they interact with the alveolar epithelium. It is therefore critical to understand the effects of human pulmonary surfactant when evaluating the inhalation toxicity of silver nanoparticles. In this study, we evaluated the toxicity of AgNPs on human alveolar type-I-like epithelial (TT1) cells in the absence and presence of Curosurf(®) (a natural pulmonary surfactant substitute), hypothesising that the pulmonary surfactant would act to modify toxicity. We demonstrated that 20nm citrate-capped AgNPs induce toxicity in human alveolar type I-like epithelial cells and, in agreement with our hypothesis, that pulmonary surfactant acts to mitigate this toxicity, possibly through reducing AgNP dissolution into cytotoxic Ag(+) ions. For example, IL-6 and IL-8 release by TT1 cells significantly increased 10.7- and 35-fold, respectively (P<0.01), 24h after treatment with 25μg/ml AgNPs. In contrast, following pre-incubation of AgNPs with Curosurf(®), this effect was almost completely abolished. We further determined that the mechanism of this toxicity is likely associated with Ag(+) ion release and lysosomal disruption, but not with increased reactive oxygen species generation. This study provides a critical understanding of the toxicity of AgNPs in target human alveolar type-I-like epithelial cells and the role of pulmonary surfactant in mitigating this toxicity. The observations reported have important implications for the manufacture and application of AgNPs, in particular for applications involving use of aerosolised AgNPs.
    Matched MeSH terms: Inflammation Mediators/metabolism
  13. Ooi TC, Chan KM, Sharif R
    Biol Trace Elem Res, 2016 Aug;172(2):458-464.
    PMID: 26749414 DOI: 10.1007/s12011-015-0615-x
    This study aimed to investigate the role of the mitogen-activated protein kinases (MAPKs) signaling pathway in the anti-inflammatory effects of zinc carnosine (ZnC) in lipopolysaccharide (LPS)-induced RAW 264.7 cells. Cells were pretreated with ZnC (0-100 μM) for 2 h prior to the addition of LPS (1 μg/ml). Following 24 h of treatment, ZnC was found not to be cytotoxic to RAW 264.7 cells up to the concentration of 100 μM. Our current findings showed that ZnC did not protect RAW 264.7 cells from LPS-induced "respiratory burst". Significant increment in intracellular glutathione (GSH) level and reduction in thiobarbituric acid reactive substances (TBARS) concentration can only be observed in cell pretreated with high doses of ZnC only (50 and 100 μM for GSH and 100 μM only for TBARS). On the other hand, pretreatment of cells with ZnC was able to inhibit LPS-induced inducible nitric oxide synthase and cyclooxygenase-2 expression significantly. Furthermore, results from immunoblotting showed that ZnC was able to suppress nuclear factor-kappaB (NF-κB) activation, and highest suppression can be observed at 100 μM of ZnC pretreatment. However, pretreatment of ZnC did not inhibit the early activation of MAPKs. In conclusion, pretreatment with ZnC was able to inhibit the expression of inflammatory mediators in LPS-induced RAW 264.7 cells, mainly via suppression of NF-κB activation, and is independent of the MAPKs signaling pathway.
    Matched MeSH terms: Inflammation Mediators/metabolism*
  14. Passmore MR, Byrne L, Obonyo NG, See Hoe LE, Boon AC, Diab SD, et al.
    Respir Res, 2018 Nov 22;19(1):231.
    PMID: 30466423 DOI: 10.1186/s12931-018-0935-4
    BACKGROUND: Sepsis is a multi-system syndrome that remains the leading cause of mortality and critical illness worldwide, with hemodynamic support being one of the cornerstones of the acute management of sepsis. We used an ovine model of endotoxemic shock to determine if 0.9% saline resuscitation contributes to lung inflammation and injury in acute respiratory distress syndrome, which is a common complication of sepsis, and investigated the potential role of matrix metalloproteinases in this process.

    METHODS: Endotoxemic shock was induced in sheep by administration of an escalating dose of lipopolysaccharide, after which they subsequently received either no fluid bolus resuscitation or a 0.9% saline bolus. Lung tissue, bronchoalveolar fluid (BAL) and plasma were analysed by real-time PCR, ELISA, flow cytometry and immunohistochemical staining to assess inflammatory cells, cytokines, hyaluronan and matrix metalloproteinases.

    RESULTS: Endotoxemia was associated with decreased serum albumin and total protein levels, with activated neutrophils, while the glycocalyx glycosaminoglycan hyaluronan was significantly increased in BAL. Quantitative real-time PCR studies showed higher expression of IL-6 and IL-8 with saline resuscitation but no difference in matrix metalloproteinase expression. BAL and tissue homogenate levels of IL-6, IL-8 and IL-1β were elevated.

    CONCLUSIONS: This data shows that the inflammatory response is enhanced when a host with endotoxemia is resuscitated with saline, with a comparatively higher release of inflammatory cytokines and endothelial/glycocalyx damage, but no change in matrix metalloproteinase levels.

    Matched MeSH terms: Inflammation Mediators/metabolism*
  15. Kinfe TM, Buchfelder M, Chaudhry SR, Chakravarthy KV, Deer TR, Russo M, et al.
    Int J Mol Sci, 2019 Sep 24;20(19).
    PMID: 31554241 DOI: 10.3390/ijms20194737
    Chronic pain is a devastating condition affecting the physical, psychological, and socioeconomic status of the patient. Inflammation and immunometabolism play roles in the pathophysiology of chronic pain disorders. Electrical neuromodulation approaches have shown a meaningful success in otherwise drug-resistant chronic pain conditions, including failed back surgery, neuropathic pain, and migraine. A literature review (PubMed, MEDLINE/OVID, SCOPUS, and manual searches of the bibliographies of known primary and review articles) was performed using the following search terms: chronic pain disorders, systemic inflammation, immunometabolism, prediction, biomarkers, metabolic disorders, and neuromodulation for chronic pain. Experimental studies indicate a relationship between the development and maintenance of chronic pain conditions and a deteriorated immunometabolic state mediated by circulating cytokines, chemokines, and cellular components. A few uncontrolled in-human studies found increased levels of pro-inflammatory cytokines known to drive metabolic disorders in chronic pain patients undergoing neurostimulation therapies. In this narrative review, we summarize the current knowledge and possible relationships of available neurostimulation therapies for chronic pain with mediators of central and peripheral neuroinflammation and immunometabolism on a molecular level. However, to address the needs for predictive factors and biomarkers, large-scale databank driven clinical trials are needed to determine the clinical value of molecular profiling.
    Matched MeSH terms: Inflammation Mediators/metabolism
  16. Taha H, Arya A, Paydar M, Looi CY, Wong WF, Vasudeva Murthy CR, et al.
    Food Chem Toxicol, 2014 Apr;66:295-306.
    PMID: 24518542 DOI: 10.1016/j.fct.2014.01.054
    The current study aimed to ascertain the antidiabetic potential of Pseuduvaria monticola bark methanolic extract (PMm) using in vitro mechanistic study models. In particular, the study determined the effect of PMm on cellular viability, 2-NBDG glucose uptake, insulin secretion, and NF-κB translocation in mouse pancreatic insulinoma cells (NIT-1). Furthermore, in vivo acute toxicity and antidiabetic studies were performed using streptozotocin (STZ)-induced type 1 and STZ-nicotinamide-induced type 2 diabetic rat models to evaluate various biochemical parameters and markers of oxidative stress and pro-inflammatory cytokines. Five isoquinoline alkaloids and three phenolic compounds were tentatively identified in the PMm by LC/MS Triple TOF. The study results showed that PMm is non-toxic to NIT-1 cells and significantly increased the glucose uptake and insulin secretion without affecting the translocation of NF-κB. Moreover, the non-toxic effects of PMm were confirmed through an in vivo acute toxicity study, which revealed that the serum insulin and C-peptide levels were significantly upregulated in type 2 diabetic rats and that no significant changes were observed in type 1 diabetic rats. Similarly, PMm was found to downregulate the levels of oxidative stress and pro-inflammatory cytokines in type 2 diabetic rats by alleviating hyperglycemia. Therefore, we conclude that PMm may be developed as an antidiabetic agent for the treatment of type 2 diabetes-associated conditions.
    Matched MeSH terms: Inflammation Mediators/metabolism
  17. Ali SS, Ahmad WANW, Budin SB, Zainalabidin S
    Rev Cardiovasc Med, 2020 Jun 30;21(2):225-240.
    PMID: 32706211 DOI: 10.31083/j.rcm.2020.02.49
    In spite of medical advances, cardiovascular disease remains a significant concern, imposing a great burden upon the economy and public health of nations by causing the highest morbidity and mortality cases globally. Moreover, it is well established that inflammation is closely linked to the pathogenesis of cardiovascular diseases. Hence, targeting inflammation seems to be a promising strategy in reducing cardiovascular risks. Currently, the importance of natural products in modern medicine is well recognised and continues to be of interest to the pharmaceutical industry. Phenolic acids are a class of phytochemical compounds that are well-known for their health benefits. They consists of various phytochemical constituents and have been widely studied in various disease models. Research involving both animals and humans has proven that phenolic acids possess cardioprotective properties such as anti-hypertensive, anti-hyperlipidemia, anti-fibrotic and anti-hypertrophy activity. Furthermore, numerous studies have proven that phenolic acids in phytochemical constituents such as gallic acid, caffeic acid and chlorogenic acid are promising anti-inflammatory agents. Hence, in this review, we outline and review recent evidence on the role of phenolic acids and their anti-inflammatory significance in studies published during the last 5 years. We also discuss their possible mechanisms of action in modulating inflammation related to cardiovascular disease.
    Matched MeSH terms: Inflammation Mediators/metabolism*
  18. Haque MA, Jantan I, Harikrishnan H, Ahmad W
    BMC Complement Med Ther, 2020 Aug 06;20(1):245.
    PMID: 32762741 DOI: 10.1186/s12906-020-03039-7
    BACKGROUND: Immunomodulatory effects of Tinospora crispa have been investigated due to its traditional use to treat several inflammatory disorders associated to the immune system. The present study reports the underlying mechanisms involved in the stimulation of 80% ethanol extract of T. crispa stems on pro-inflammatory mediators release in lipopolysaccharide (LPS)-primed U937 human macrophages via MyD88-dependent pathways.

    METHODS: Release of interleukin (IL)-1β and tumor necrosis factor (TNF)-α, and production of prostaglandin E2 (PGE2) were determined by using enzyme-linked immunosorbent assay (ELISA). Immunoblot technique was executed to determine the activation of MAPKs molecules, NF-κB, PI3K-Akt and cyclooxygenase-2 (COX-2) protein. Determination of pro-inflammatory cytokines and COX-2 relative gene expression levels was by performing the real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). A reversed-phase HPLC method was developed and validated to standardize the T. crispa extract and chemical profiling of its secondary metabolites was performed by LC-MS/MS.

    RESULTS: Qualitative and quantitative analyses of chromatographic data indicated that syringin and magnoflorine were found as the major components of the extract. T. crispa-treatment prompted activation of NF-κB by enhancing IKKα/β and NF-κB (p65) phosphorylation, and degradation of IκBα. The extract upregulated COX-2 protein expression, release of pro-inflammatory mediators and MAPKs (ERK, p38 and JNK) phosphorylation as well as Akt dose-dependently. T. crispa extract also upregulated the upstream signaling adaptor molecules, toll-like receptor 4 (TLR4) and MyD88. T. crispa-treatment also upregulated the pro-inflammatory markers mRNA expression.

    CONCLUSION: The results suggested that T. crispa extract stimulated the MyD88-dependent signaling pathways by upregulating the various immune inflammatory related parameters.

    Matched MeSH terms: Inflammation Mediators/metabolism*
  19. Al-Fahdawi MQ, Al-Doghachi FAJ, Abdullah QK, Hammad RT, Rasedee A, Ibrahim WN, et al.
    Biomed Pharmacother, 2021 Jun;138:111483.
    PMID: 33744756 DOI: 10.1016/j.biopha.2021.111483
    The aim of this study was to prepare, characterize, and determine the in vitro anticancer effects of platinum-doped magnesia (Pt/MgO) nanoparticles. The chemical compositions, functional groups, and size of nanoparticles were determined using X-ray diffraction, Fourier transform infrared spectroscopy, energy dispersive X-ray spectroscopy, transmission electron microscopy, and scanning electron microscopy. Pt/MgO nanoparticles were cuboid and in the nanosize range of 30-50 nm. The cytotoxicity of Pt/MgO nanoparticles was determined via the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay on the human lung and colonic cancer cells (A549 and HT29 respectively) and normal human lung and colonic fibroblasts cells (MRC-5 and CCD-18Co repectively). The Pt/MgO nanoparticles were relatively innocuous to normal cells. Pt/MgO nanoparticles downregulated Bcl-2 and upregulated Bax and p53 tumor suppressor proteins in the cancer cells. Pt/MgO nanoparticles also induced production of reactive oxygen species, decreased cellular glutathione level, and increased lipid peroxidation. Thus, the anticancer effects of Pt/MgO nanoparticles were attributed to the induction of oxidative stress and apoptosis. The study showed the potential of Pt/MgO nanoparticles as an anti-cancer compound.
    Matched MeSH terms: Inflammation Mediators/metabolism
  20. Ranneh Y, Akim AM, Hamid HA, Khazaai H, Mokhtarrudin N, Fadel A, et al.
    Arch Immunol Ther Exp (Warsz), 2019 Dec;67(6):385-400.
    PMID: 31278602 DOI: 10.1007/s00005-019-00553-6
    Chronic subclinical systemic inflammation has a key role in stimulating several chronic conditions associated with cardiovascular diseases, cancer, rheumatoid arthritis, diabetes, and neurodegenerative diseases. Hence, developing in vivo models of chronic subclinical systemic inflammation are essential to the study of the pathophysiology and to measure the immunomodulatory agents involved. Male Sprague-Dawley rats were subjected to intraperitoneal, intermittent injection with saline, or lipopolysaccharide (LPS) (0.5, 1, 2 mg/kg) thrice a week for 30 days. Hematological, biochemical, and inflammatory mediators were measured at different timepoints and at the end of the study. The hearts, lungs, kidneys, and livers were harvested for histological evaluation. Significant elevation in peripheral blood leukocyte includes neutrophils, monocytes, and lymphocytes, as well as the neutrophils-to-lymphocyte ratio. The pro-inflammatory mediator levels [C-reactive protein, tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and IL-8] along with the biochemical profile (alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl transferase, creatine kinase, creatinine, and urea) were increased significantly (P 
    Matched MeSH terms: Inflammation Mediators/metabolism
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