Displaying publications 1 - 20 of 271 in total

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  1. Harun NH, Froemming GRA, Mohd Ismail A, Nawawi H, Mokhtar SS, Abd Muid S
    Int J Mol Sci, 2022 Nov 23;23(23).
    PMID: 36498945 DOI: 10.3390/ijms232314616
    Low mineralization activity by human osteoblast cells (HOBs) indicates abnormal bone remodeling that potentially leads to osteoporosis. Oxidation, the most prominent form of high-density lipoprotein (HDL) modification, is suggested to affect bone mineralization through the inflammatory pathway. Adiponectin, which possesses anti-inflammatory activity, is postulated to have the ability to suppress the detrimental effects of oxidized HDL (oxHDL). This study aimed to investigate the effects of HDL before and after oxidation on markers of mineralization and inflammation. The protective effects of adiponectin on demineralization and inflammation induced by oxHDL were also investigated. OxHDL at 100 µg/mL protein had the highest inhibitory effect on mineralization, followed by lower calcium incorporation. OxHDL also had significantly lower expression of a mineralization marker (COL1A2) and higher expression of inflammatory markers (IL-6, TNF-α, and RELA proto-oncogene, NF-κβ (p65)) compared to the unstimulated control group. These findings suggest that oxHDL reduces the mineralization activity of HOBs by increasing the expression of inflammatory markers. Interestingly, co-incubation of adiponectin and oxHDL in HOBs resulted in higher expression of mineralization markers (ALPL, COL1A2, BGLAP, and RUNX2) and significantly reduced all targeted inflammatory markers compared to the oxHDL groups. On the contrary, HDL increased the expression of mineralization markers (COL1A2 and STAT-3) and exhibited lower expression of inflammatory cytokines (IL-6 and TNF-α), proving the protective effect of HDL beyond the reverse cholesterol transport activity.
    Matched MeSH terms: Tumor Necrosis Factor-alpha
  2. Fathy SA, Mohamed MR, Emam MA, Mohamed SS, Ghareeb DA, Elgohary SA, et al.
    Trop Biomed, 2019 Dec 01;36(4):972-986.
    PMID: 33597467
    Candida is the most frequent common causes of invasive fungal infections and associated with high morbidity and mortality. Most of available antifungal agents have side effects. This opened up new avenues to investigate the antifungal efficacy of active extracts from marine algae. So the aim of this study was to evaluate the protective and the curative effect of Ulva fasciata extract against an invasive candidiasis in mice and to study its underlying mechanism. The active ingredients of Ulva fasciata extract were evaluated using HPLC and GC/MS. Fifty mice were included in current work, and the level of inflammatory markers; Interleukin (IL)-4, IL-12, Interferon-gamma (IFN-γ) and Tumor necrosis factor-alpha (TNF-α) were determined using ELISA kits. Hematological, biochemical and oxidative stress parameters were determined using commercial kits. Moreover, the histopathological examinations were carried on liver, kidney and spleen for all groups. The results obtained showed that treatment with U. fasciata either before or after Candida infection significantly improved the hematological, biochemical alterations and antioxidant status caused by this infection. Furthermore, the U. fasciata reduced histopathological changes induced by Candida as well as it could increase the expression of IL-12 and IFN-γ while minimized the expression of TNF-α and IL-4 in all infected mice compared to infected untreated mice. These data propose that U. fasciata can ameliorate inflammatory reactions related to Candida albicans cytotoxicity via its ability to augment cellular antioxidant defenses by its active compounds.
    Matched MeSH terms: Tumor Necrosis Factor-alpha/metabolism
  3. Salga MS, Ali HM, Abdulla MA, Abdelwahab SI
    Chem Biol Interact, 2012 Jan 25;195(2):144-53.
    PMID: 22178775 DOI: 10.1016/j.cbi.2011.11.008
    Zinc complexes were reported to have anti-ulcer activity and used as drug for the treatment of gastrointestinal disorders. A novel compound dichlorido-zinc(II)-4-(2-(5-methoxybenzylidene amino)ethyl)piperazin-1-iumphenolate (ZnHMS) was synthesized, characterized and evaluated for its gastroprotective activity against ethanol-induced ulcer in rats. Gross and microscopic lesions, histochemical staining of glycogen storage, biochemical and immunological parameters were taken into consideration. Oral administration of ZnHMS (30 and 60 mg/kg; 14 days) dose-dependently inhibited gastric lesions. It significantly increased the mucus content and total acidity compared to the control group (P<0.01). Serum levels of aspartate (AST), alanine (ALT) transaminases, pro-inflammatory interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and anti-inflammatory interleukin-10 (IL-10) in the rats exposed to ethanol induced ulceration have been altered. ZnHMS considerably enhances (P<0.05) the protection of gastric epithelia by modulating the acute alterations of AST, ALT, IL-6, IL-10, TNF-α and stomach glycogen. Interestingly, ZnHMS did interfere with the natural release of nitric oxide. In addition, acute toxicity study revealed no abnormal sign to the rats treated with ZnHMS (2000 mg/kg). These findings suggest that the gastroprotective activity of ZnHMS might contribute in adjusting the inflammatory cytokine-mediated oxidative damage to the gastric mucosa.
    Matched MeSH terms: Tumor Necrosis Factor-alpha/metabolism
  4. Ban EZ, Lye MS, Chong PP, Yap YY, Lim SYC, Abdul Rahman H
    PLoS One, 2018;13(6):e0198332.
    PMID: 29912899 DOI: 10.1371/journal.pone.0198332
    BACKGROUND: Nasopharyngeal carcinoma is a rare form of cancer across the world except in certain areas such as Southern China, Hong Kong and Malaysia. NPC is considered a relatively radiosensitive tumor and patients diagnosed at early stages tend to survive longer compared to those with advanced disease. Given that early symptoms of NPC are non-specific and that the nasopharynx is relatively inaccessible, less invasive screening methods such as biomarker screening might be the key to improve NPC survival and management. A number of genes with their respective polymorphisms have been shown in past studies to be associated with survival of various cancers. hOGG1 and XPD genes encode for a DNA glycosylase and a DNA helicase respectively; both are proteins that are involved in DNA repair. ITGA2 is the alpha subunit of the transmembrane receptor integrin and is mainly responsible for cell-cell and cell-extracellular matrix interaction. TNF-α is a cytokine that is released by immune cells during inflammation.

    METHODS: Restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) was used to genotype all the aforementioned gene polymorphisms. Kaplan-Meier survival function, log-rank test and Cox regression were used to investigate the effect of gene polymorphisms on the all-cause survival of NPC.

    RESULTS: NPC cases carrying T/T genotype of ITGA2 C807T have poorer all-cause survival compared to those with C/C genotypes, with an adjusted HR of 2.06 (95% CI = 1.14-3.72) in individual model. The 5-year survival rate of C/C carriers was 55% compared to those with C/T and T/T where the survival rates were 50% and 43%, respectively.

    CONCLUSION: The finding from the present study showed that ITGA2 C807T polymorphism could be potentially useful as a prognostic biomarker for NPC. However, the prognostic value of ITGA2 C807T polymorphism has to be validated by well-designed further studies with larger patient numbers.

    Matched MeSH terms: Tumor Necrosis Factor-alpha/genetics*
  5. Dhiyaaldeen SM, Alshawsh MA, Salama SM, Alwajeeh NS, Al Batran R, Ismail S, et al.
    Biomed Res Int, 2014;2014:792086.
    PMID: 24587992 DOI: 10.1155/2014/792086
    Wound healing involves inflammation followed by granular tissue development and scar formation. In this study, synthetic chalcone 3-(2-Chlorophenyl)-1-phenyl-propenone (CPPP) was investigated for a potential role in enhancing wound healing and closure. Twenty-four male rats were divided randomly into 4 groups: carboxymethyl cellulose (CMC) (0.2 mL), Intrasite gel, and CPPP (25 or 50 mg/mL). Gross morphology, wounds treatment with the CPPP, and Intrasite gel accelerate the rate of wound healing compared to CMC group. Ten days after surgery, the animals were sacrificed. Histological assessment revealed that the wounds treated with CPPP showed that wound closure site contained little amount of scar and the granulation tissue contained more collagen and less inflammatory cells than wound treated with CMC. This finding was confirmed with Masson's trichrome staining. The antioxidant defence enzymes catalase (CAT) and superoxide dismutase (SOD) were significantly increased in the wound homogenates treated with CPPP (P < 0.05) compared to CMC treated group. However, in the CPPP treatment group, lipid peroxidation (MDA) was significantly decreased (P < 0.05), suggesting that the CPPP also has an important role in protection against lipid peroxidation-induced skin injury after ten days of treatment with CPPP, which is similar to the values of cytokines TGF-β and TNF-α in tissue homogenate. Finally the administration of CPPP at a dosage of 25 and 50 mg/kg was suitable for the stimulation of wound healing.
    Matched MeSH terms: Tumor Necrosis Factor-alpha/metabolism
  6. Hong CY, Wong NK, Abdullah M
    Asian Pac J Allergy Immunol, 2015 Mar;33(1):26-32.
    PMID: 25840631 DOI: 10.12932/AP0463.33.1.2015
    Tamm-Horsfall glycoprotein (THP) and uromodulin are the most abundant glycoproteins in non-pregnant women's/men's and pregnant women's urine, respectively. However, the bioactivities of these glycoproteins are still unclear.
    Matched MeSH terms: Tumor Necrosis Factor-alpha/biosynthesis; Tumor Necrosis Factor-alpha/secretion
  7. Batumalaie K, Amin MA, Murugan DD, Sattar MZ, Abdullah NA
    Sci Rep, 2016 06 02;6:27236.
    PMID: 27250532 DOI: 10.1038/srep27236
    Activation of inflammatory pathways via reactive oxygen species (ROS) by free fatty acids (FFA) in obesity gives rise to insulin resistance and endothelial dysfunction. Withaferin A (WA), possesses both antioxidant and anti-inflammatory properties and therefore would be a good strategy to suppress palmitic acid (PA)-induced oxidative stress and inflammation and hence, insulin resistance and dysfunction in the endothelium. Effect of WA on PA-induced insulin resistance in human umbilical vein endothelial cells (HUVECs) was determined by evaluating insulin signaling mechanisms whilst effect of this drug on PA-induced endothelial dysfunction was determined in acetylcholine-mediated relaxation in isolated rat aortic preparations. WA significantly inhibited ROS production and inflammation induced by PA. Furthermore, WA significantly decreased TNF-α and IL-6 production in endothelial cells by specifically suppressing IKKβ/NF-κβ phosphorylation. WA inhibited inflammation-stimulated IRS-1 serine phosphorylation and improved the impaired insulin PI3-K signaling, and restored the decreased nitric oxide (NO) production triggered by PA. WA also decreased endothelin-1 and plasminogen activator inhibitor type-1 levels, and restored the impaired endothelium-mediated vasodilation in isolated aortic preparations. These findings suggest that WA inhibited both ROS production and inflammation to restore impaired insulin resistance in cultured endothelial cells and improve endothelial dysfunction in rat aortic rings.
    Matched MeSH terms: Tumor Necrosis Factor-alpha/metabolism
  8. Sucedaram Y, Johns EJ, Husain R, Abdul Sattar M, H Abdulla M, Nelli G, et al.
    J Inflamm Res, 2021;14:689-710.
    PMID: 33716510 DOI: 10.2147/JIR.S299083
    Purpose: We hypothesized that low estrogen levels aggravate obesity-related complications. Diet-induced obesity can cause distinct pathologies, including impaired glucose tolerance, inflammation, and organ injury that leads to fatty liver and chronic kidney diseases. To test this hypothesis, ovariectomized (OVX) rats were fed a high-fat style diet (HFSD), and we examined structural changes and inflammatory response in the kidney and liver.

    Methods: Sprague-Dawley female rats were ovariectomized or sham-operated and divided into four groups: sham-operated rats fed a normal diet (ND); ovariectomized rats fed a normal diet (OVX-ND); sham-operated rats fed a HFSD; ovariectomized rats fed a high-fat style diet (OVX-HFSD). Mean blood pressure and fasting blood glucose were measured on weeks 0 and 10. The rats were sacrificed 10 weeks after initiation of ND or HFSD, the kidney and liver were harvested for histological, immunohistochemical and immunofluorescence studies.

    Results: HFSD-fed rats presented a significantly greater adiposity index compared to their ND counterparts. Liver index, fasting blood glucose and mean blood pressure was increased in OVX-HFSD rats compared to HFSD rats at study terminal. Histological and morphometric studies showed focal interstitial mononuclear cell infiltration in the kidney of HFSD rats with mesangial expansion being greater in the OVX-HFSD rats. Both HFSD fed groups showed increased expressions of renal inflammatory markers, namely TNF-alpha, IL-6 and MCP-1, and infiltrating M1 macrophages with some influence of ovarian hormonal status. HFSD-feeding also caused hepatocellular steatosis which was aggravated in ovariectomized rats fed the same diet. Furthermore, hepatocellular ballooning was observed only in the OVX-HFSD rats. Similarly, HFSD-fed rats showed increased expressions of the inflammatory markers and M1 macrophage infiltration in the liver; however, only IL-6 expression was magnified in the OVX-HFSD.

    Conclusion: Our data suggest that some of the structural changes and inflammatory response in the kidney and liver of rats fed a HFSD are exacerbated by ovariectomy.

    Matched MeSH terms: Tumor Necrosis Factor-alpha
  9. Che Noh I, Avoi R, Abdullah Nurul A, Ahmad I, Abu Bakar R
    PeerJ, 2022;10:e13330.
    PMID: 35469194 DOI: 10.7717/peerj.13330
    BACKGROUND: Chronic hepatitis C virus (HCV) infection is one of the major causes of liver cirrhosis and liver carcinoma. Studies have indicated that an imbalance of cytokine activities could contribute to the pathogenesis of chronic HCV infection. This study aimed to investigate serum levels and gene expression of cytokines (IL-6, TNF-α and TGF-β1) in chronic HCV infection among Malay male subjects.

    METHODS: Thirty-nine subjects were enrolled from various health clinics in Kelantan, Malaysia, and divided into two groups: patients with chronic HCV infection (HP) and healthy control (HS). The serum cytokines IL-6, TNF-a-were measured using Luminex assay, and serum TGF-β1 was measured by ELISA. The mRNA gene expression for IL-6, TNF-α and TGF-β1 was measured by real-time reverse transcriptase polymerase chain reaction (RT-PCR).

    RESULTS: There were statistically significant differences in the mean serum levels of IL-6, and TGF-β1 in HP compared to HS group (p = 0.0180 and p = 0.0005, respectively). There was no significant difference in the mean serum level of TNF-α in HP compared to HS group. The gene expression for the studied cytokines showed no significant differences in HP compared to HS group.

    CONCLUSION: Serum IL-6 was significantly associated with chronic HCV infection.

    Matched MeSH terms: Tumor Necrosis Factor-alpha/genetics
  10. Sam SS, Teoh BT, Chinna K, AbuBakar S
    Int J Med Sci, 2015;12(2):177-86.
    PMID: 25589894 DOI: 10.7150/ijms.8988
    Dengue virus (DENV) infection usually presents with mild self-limiting dengue fever (DF). Few however, would present with the more severe form of the disease, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). In the present study, the association between IL-12B, IL-10 and TNF-α gene polymorphisms and dengue severity was investigated.
    METHODS: A case-control study was performed on a total of 120 unrelated controls, 86 DF patients and 196 DHF/DSS patients. The polymorphisms in IL-12B, IL-10 and TNF-α genes were genotyped using PCR-RFLP and PCR-sequencing methods.
    RESULTS: A protective association of TNF-α -308A allele and -308GA genotype against DHF/DSS was observed, while TNF-α -238A allele and -238GA genotype were associated with DHF/DSS. A combination of TNF-α -308GA+AA genotype and IL-10 non-GCC haplotypes, IL-12B pro homozygotes (pro1/pro1, pro2/pro2) and IL-12B 3'UTR AC were significantly correlated with protective effects against DHF/DSS. An association between the cytokine gene polymorphisms and protection against the clinical features of severe dengue including thrombocytopenia and increased liver enzymes was observed in this study.
    CONCLUSION: The overall findings of the study support the correlation of high-producer TNF-α genotypes combined with low-producer IL-10 haplotypes and IL-12B genotypes in reduced risk of DHF/DSS.
    KEYWORDS: Infectious disease; cytokine; dengue; genetics; polymorphism.; tropical
    Matched MeSH terms: Tumor Necrosis Factor-alpha/genetics*
  11. Shu MH, Appleton D, Zandi K, AbuBakar S
    PMID: 23497105 DOI: 10.1186/1472-6882-13-61
    Gracilaria changii (Xia et Abbott) Abbott, Zhang et Xia, a red algae commonly found in the coastal areas of Malaysia is traditionally used for foods and for the treatment of various ailments including inflammation and gastric ailments. The aim of the study was to investigate anti-inflammatory, gastroprotective and anti-ulcerogenic activities of a mass spectrometry standardized methanolic extract of Gracilaria changii.
    Matched MeSH terms: Tumor Necrosis Factor-alpha/genetics; Tumor Necrosis Factor-alpha/metabolism
  12. Wong PF, Jamal J, Tong KL, Khor ES, Yeap CE, Jong HL, et al.
    Microvasc Res, 2017 11;114:26-33.
    PMID: 28595801 DOI: 10.1016/j.mvr.2017.06.002
    miRNAs are important regulators of cellular senescence yet the extent of their involvement remains to be investigated. We sought to identify miRNAs that are involved in cytokine-induced premature senescence (CIPS) in endothelial cells. CIPS was established in young human pulmonary microvascular endothelial cells (HMVEC-Ls) following treatment with a sublethal dose (20ng/ml) of tumor necrosis factor alpha (TNF-α) for 15days. In parallel, HMVEC-Ls were grown and routinely passaged until the onset of replicative senescence (RS). Differential expression analysis following miRNA microarray profiling revealed an overlapped of eight deregulated miRNAs in both the miRNA profiles of RS and TNF-α-induced premature senescence cells. Amongst the deregulated miRNAs were members of the miR 17-92 cluster which are known regulators of angiogenesis. The role of hsa-miR-20b in TNF-α-induced premature senescence, a paralog member of the miR 17-92 cluster, was further investigated. Biotin-labeled hsa-miR-20b captured the enriched transcripts of retinoblastoma-like 1 (RBL1), indicating that RBL1 is a target of hsa-miR-20b. Knockdown of hsa-miR-20b attenuated premature senescence in the TNF-α-treated HMVEC-Ls as evidenced by increased cell proliferation, increased RBL1 mRNA expression level but decreased protein expression of p16INK4a, a cellular senescence marker. These findings provide an early insight into the role of hsa-miR-20b in endothelial senescence.
    Matched MeSH terms: Tumor Necrosis Factor-alpha/pharmacology*
  13. Majeed AY, Zulkafli NES, Ad'hiah AH
    Immunol Lett, 2023 Aug;260:24-34.
    PMID: 37339685 DOI: 10.1016/j.imlet.2023.06.008
    This study attempted to explore pro-inflammatory and anti-inflammatory responses in patients with mild/moderate coronavirus disease 19 (COVID-19). Eight pro-inflammatory (IL-1α, IL-1β, IL-12, IL-17A, IL-17E, IL-31, IFN-γ and TNF-α) and three anti-inflammatory (IL-1Ra, IL-10 and IL-13) cytokines, as well as two chemokines (CXCL9 and CXCL10), were analyzed in the serum from ninety COVID-19 patients and healthy controls. Cytokine/chemokine levels were measured using enzyme-linked immunosorbent assay kits. Results revealed that IL-1α, IL-1β, IL-10, IL-12, IL-13, IL-17A, IL-31, IFN-γ, TNF-α and CXCL10 were significantly higher in patients than in controls, while IL-1Ra levels were significantly lower in patients. IL-17E and CXCL9 levels showed no significant differences between patients and controls. Seven cytokines/chemokines recorded an area under the curve greater than 0.8: IL-12 (0.945), IL-17A (0.926), CXCL10 (0.909), IFN-γ (0.904), IL-1α (0.869), TNF-α (0.825) and IL-10 (0.821). As indicated by the odds ratio, elevated levels of nine cytokines/chemokines were associated with an increased risk of COVID-19: IL-1α (19.04), IL-10 (5.01), IL-12 (43.66), IL-13 (4.25), IL-17A (16.62), IL-31 (7.38), IFN-γ (13.55), TNF-α (12.00) and CXCL10 (11.18). Only one positive (IL-17E with TNF-α) and six negative (IL-1β, IL-17A and IL-17E with CXCL9, IL-10 with IL-17A, and IL-1β and IL-17A with CXCL10) correlations were found between these cytokines/chemokines. In conclusion, pro-inflammatory (IL-1α, IL-1β, IL-12, IL-13, IL-17A, IL-31, IFN-γ, TNF-α and CXCL10) and anti-inflammatory (IL-10 and IL-13) cytokines/chemokines were up-regulated in the serum of patients with mild/moderate COVID-19. Their potential as biomarkers for diagnosis and prognosis is suggested and the association with COVID-19 risk is indicated to give more insight on COVID-19 immunological responses among non-hospitalized patients.
    Matched MeSH terms: Tumor Necrosis Factor-alpha
  14. Mohd-Radzman NH, Ismail WI, Adam Z, Jaapar SS, Adam A
    PMID: 24324517 DOI: 10.1155/2013/718049
    Insulin resistance is a key factor in metabolic disorders like hyperglycemia and hyperinsulinemia, which are promoted by obesity and may later lead to Type II diabetes mellitus. In recent years, researchers have identified links between insulin resistance and many noncommunicable illnesses other than diabetes. Hence, studying insulin resistance is of particular importance in unravelling the pathways employed by such diseases. In this review, mechanisms involving free fatty acids, adipocytokines such as TNF α and PPAR γ and serine kinases like JNK and IKK β , asserted to be responsible in the development of insulin resistance, will be discussed. Suggested mechanisms for actions in normal and disrupted states were also visualised in several manually constructed diagrams to capture an overall view of the insulin-signalling pathway and its related components. The underlying constituents of medicinal significance found in the Stevia rebaudiana Bertoni plant (among other plants that potentiate antihyperglycemic activities) were explored in further depth. Understanding these factors and their mechanisms may be essential for comprehending the progression of insulin resistance towards the development of diabetes mellitus.
    Matched MeSH terms: Tumor Necrosis Factor-alpha
  15. Hafiz ZZ, Amin M'M, Johari James RM, Teh LK, Salleh MZ, Adenan MI
    Molecules, 2020 Feb 17;25(4).
    PMID: 32079355 DOI: 10.3390/molecules25040892
    Centella asiatica (C. asiatica) is one of the medicinal plants that has been reported to exert comprehensive neuroprotection in vitro and in vivo. In view of this, the present study was performed to investigate the effect of ethanolic extract of C. asiatica, designated as raw-extract of C. asiatica (RECA) in reducing the acetylcholinesterase (AChE), inflammations, and oxidative stress activities via both in vitro (SH-SY5Y and RAW 264.7 cells) and in vivo (Sprague Dawley rats). Quantitative high-performance liquid chromatography analysis reveals that RECA contains a significantly high proportion of glycosides than the aglycones with madecassoside as the highest component, followed by asiaticoside. Treatment of SH-SY5Y cells with RECA significantly reduced the AChE activity in a concentration-dependent manner with an IC50 value of 31.09 ± 10.07 µg/mL. Furthermore, the anti-inflammatory and antioxidant effects of RECA were evaluated by lipopolysaccharides (LPS)-stimulated RAW 264.7 cells. Our results elucidated that treatment with RECA significantly suppressed the level of pro-inflammatory cytokine/mediators and oxidative stress released in a concentration-dependent manner. Interestingly, these patterns of inhibition were consistent as observed in the LPS-induced neuroinflammation Sprague Dawley rats' model. The highest concentration used in the two models presented the most significant results. Herein, our findings strongly suggest that RECA may offer therapeutic potential for the treatment of Alzheimer's disease through inhibiting the AChE, inflammation, and oxidative stress activities.
    Matched MeSH terms: Tumor Necrosis Factor-alpha/metabolism
  16. Banerjee R, Ali RAR, Wei SC, Adsul S
    Gut Liver, 2020 11 15;14(6):685-698.
    PMID: 33191310 DOI: 10.5009/gnl19209
    The advent of biologics and biologic therapy has transformed the management of inflammatory bowel disease (IBD) with enhanced early and adequate responses to treatment, fewer hospitalizations, a reduced need for surgery, and unprecedented outcomes including complete mucosal and histologic healing. However, an important issue with the use of anti-tumor necrosis factor (anti-TNF) agents in IBD is the increased risk of tuberculosis (TB). This is compounded by the diagnostic dilemma when differentiating between Crohn's disease and gastrointestinal TB, and the potentially serious consequences of initiating an incorrect treatment in the case of misdiagnosis. The interplay between IBD and TB is most relevant in Asia, where more than 60% of the 10.4 million new TB cases in 2016 were reported. A number of studies have reported an increased risk of TB with anti-TNF agents, including in patients who had tested negative for TB prior to treatment initiation. The limited evidence currently available regarding adhesion molecule antagonists such as vedolizumab suggests a comparatively lower risk of TB, thus making them a promising option for IBD management in TBendemic regions. This comprehensive review examines the available literature on the risk of TB with the use of biologics in the TB-endemic regions of Asia, focusing on the diagnostic dilemma, the risk of reactivation, and the optimized management algorithms for latent and active disease.
    Matched MeSH terms: Tumor Necrosis Factor-alpha
  17. Agarwal R, Agarwal P
    Indian J Ophthalmol, 2012 Jul;60(4):255-61.
    PMID: 22824592 DOI: 10.4103/0301-4738.98700
    Glaucoma, a neurodegenerative disease, is currently being treated by modulation of one of its primary risk factors, the elevated intraocular pressure. Newer therapies that can provide direct neuroprotection to retinal ganglion cells are being extensively investigated. Tumor necrosis factor-α, a cytokine, has been recognized to play an important role in pro and antiapoptotic cellular events. In this paper we review the relevant literature to understand (1) The association of increased expression of tumor necrosis factor-α with glaucomatous neurodegeneraion, (2) Modulation of tumor necrosis factor-α expression by exposure to various risk factors of glaucoma, (3) Downstream cellular signaling mechanisms following interaction of tumor necrosis factor-α with its receptors and (4) Role of tumor necrosis factor-α as a possible target for therapeutic intervention in glaucoma. Literature was reviewed using PubMed search engine with relevant key words and a total of 82 English language papers published from 1990 to 2010 are included in this review.
    Matched MeSH terms: Tumor Necrosis Factor-alpha/biosynthesis*
  18. Umar MI, Asmawi MZ, Sadikun A, Majid AM, Al-Suede FS, Hassan LE, et al.
    Clinics (Sao Paulo), 2014 Feb;69(2):134-44.
    PMID: 24519205 DOI: 10.6061/clinics/2014(02)10
    The present study aimed to investigate the mechanisms underlying the anti-inflammatory and anti-angiogenic effects of ethyl-p-methoxycinnamate isolated from Kaempferia galanga.
    Matched MeSH terms: Tumor Necrosis Factor-alpha/analysis; Tumor Necrosis Factor-alpha/drug effects
  19. Alkadi KAA, Ashraf K, Adam A, Shah SAA, Taha M, Hasan MH, et al.
    J Pharm Bioallied Sci, 2020 12 21;13(1):116-122.
    PMID: 34084057 DOI: 10.4103/jpbs.JPBS_279_19
    Objectives: The aim of the present study was to isolate and evaluate cytotoxicity and anti-inflammatory activities of new novel compounds isolated from Prismatomeris glabra.

    Materials and Methods: Dried root of P. glabra was extracted under reflux with methyl alcohol, fractionated through the vacuum liquid chromatography technique, and evaporated and then purified the compounds using column chromatography and preparative thin-layer chromatography. THP-1 cells were treated with amentoflavone, 5,7,4'-hydroxyflavonoid, and stigmasterol with various concentrations (0-30 µg/mL) and then incubated with MTS reagent for 2h. Treatment was done for 24, 48, and 72h. Then, effects of these compounds were also tested on PGE2, TNF-α, and IL-6 expression in human THP-1-derived macrophage cells for 24h.

    Results: Three new compounds such as amentoflavone, 5,7,4'-hydroxyflavonoid, and stigmasterol were isolated. After 24h of incubation, a significant decrease in cell viability was reported with IC50 values of amentoflavone, 5,7,4'- hydroxyflavonoid, and stigmasterol (21 µg/mL ≡ 38 M), (18 µg/mL ≡ 66 M) and (20 µg/mL ≡ 48.5 M), respectively. Whereas for 48 and 72h treatment showed a less decreased cell viability compared with 24h treatment. These compounds also showed a significant reduction in the production of TNF-α, IL-6, and PGE2 in a dose-dependent manner.

    Conclusions: The isolated new compounds showed significant cytotoxicity and anti-inflammatory effects.

    Matched MeSH terms: Tumor Necrosis Factor-alpha
  20. Fong LY, Ng CT, Yong YK, Hakim MN, Ahmad Z
    Vascul. Pharmacol., 2019 06;117:15-26.
    PMID: 30114509 DOI: 10.1016/j.vph.2018.08.005
    Endothelial hyperpermeability represents an initiating step in early atherosclerosis and it often occurs as a result of endothelial barrier dysfunction. Asiatic acid, a major triterpene isolated from Centella asiatica (L.) Urban, has previously been demonstrated to protect against tumor necrosis factor (TNF)-α-induced endothelial barrier dysfunction. The present study aimed to investigate the mechanisms underlying the barrier protective effect of asiatic acid in human aortic endothelial cells (HAECs). The localization of F-actin, diphosphorylated myosin light chain (diphospho-MLC), adherens junctions (AJs) and tight junctions (TJs) was studied using immunocytochemistry techniques and confocal microscopy. Their total protein expressions were examined using western blot analysis. The endothelial permeability was assessed using In Vitro Vascular Permeability Assay kits. In addition, intracellular redistribution of the junctional proteins was evaluated using subcellular fractionation kits. We show that asiatic acid stabilized F-actin and diphospho-MLC at the cell periphery and prevented their rearrangement stimulated by TNF-α. However, asiatic acid failed to attenuate cytochalasin D-induced increased permeability. Besides, asiatic acid abrogated TNF-α-induced structural reorganization of vascular endothelial (VE)-cadherin and β-catenin by preserving their reticulum structures at cell-cell contact areas. In addition, asiatic acid also inhibited TNF-α-induced redistribution of occludin and zona occludens (ZO)-1 in different subcellular fractions. In conclusion, the barrier-stabilizing effect of asiatic acid might be associated with preservation of AJs and prevention of TJ redistribution caused by TNF-α. This study provides evidence to support the potential use of asiatic acid in the prevention of early atherosclerosis, which is initiated by endothelial barrier dysfunction.
    Matched MeSH terms: Tumor Necrosis Factor-alpha/pharmacology*
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