Tumor Necrosis Factor (TNF) Alpha Inhibitor https://greenmedinfo.com/category/keywords/Tumor%20Necrosis%20Factor%20%28TNF%29%20Alpha%20Inhibitor en A combination of aerobic exercise and resistance training was effective in reducing inflammation. https://greenmedinfo.com/article/combination-aerobic-exercise-and-resistance-training-was-effective-reducing-in n/a PMID:  J Phys Act Health. 2017 Mar 2:1-22. Epub 2017 Mar 2. PMID: 28253046 Abstract Title:  Effect of Moderate Intensity Exercise on Inflammatory Markers Among Postmenopausal Women. Abstract:  BACKGROUND: Declines in ovarian function in postmenopausal women may contribute to increase inflammatory cytokines, which can lead to chronic diseases. However, studies have shown that exercise interventions are important to manage inflammatory conditions. Thus, the objective of this study was to analyze the effect of exercise intervention on inflammatory markers among obese and postmenopausal women. METHODS: 70 women composed the sample (Exercise group [EG; n=35] and non-exercise group [nEG; n=35]). IL-6, TNF-α and IL-10 were the inflammatory markers analyzed. Exercise program was 20 weeks long and consisted of aerobic and neuromuscular training. Data about chronic diseases, medication use, dietary intake, body composition and biochemical variables were collected. RESULTS: EG showed significant reductions in body mass index, waist circumference and body fat percentage, as well as increased lean body mass. EG showed significant reductions in TNF-α and significant interaction between group and intervention time. Reductions in IL-10 were identified only in nEG. Substantial effect of exercise intervention was observed with increased ratio of IL-10/IL-6 and IL-10/TNF-α. CONCLUSIONS: Combination of aerobic exercise and resistance training was effective in reducing inflammation. Thus, implementation and maintenance of similar exercise programs can contribute to reduce chronic inflammation among obese postmenopausal women. https://greenmedinfo.com/article/combination-aerobic-exercise-and-resistance-training-was-effective-reducing-in#comments Inflammation Postmenopausal Complications Anti-Inflammatory Agents Exercise: Aerobic Exercise: Resistance Training Tumor Necrosis Factor (TNF) Alpha Inhibitor Anti-Inflammatory Agents Exercise: Aerobic Exercise: Resistance Training Inflammation Postmenopausal Complications Tumor Necrosis Factor (TNF) Alpha Inhibitor Human Study Wed, 08 Mar 2017 01:52:00 +0000 greenmedinfo 144505 at https://greenmedinfo.com Baicalein could be a lead compound for the modulation of inflammatory diseases as well as certain cancers. https://greenmedinfo.com/article/baicalein-could-be-lead-compound-modulation-inflammatory-diseases-well-certain n/a PMID:  Oncol Rep. 2016 Nov ;36(5):2771-2776. Epub 2016 Aug 19. PMID: 27667548 Abstract Title:  Baicalein inhibits TNF-α-induced NF-κB activation and expression of NF-κB-regulated target gene products. Abstract:  The nuclear factor-κB (NF-κB) transcription factors control many physiological processes including inflammation, immunity, apoptosis and angiogenesis. In our search for NF-κB inhibitors from natural resources, we identified baicalein from Scutellaria baicalensis as an inhibitor of NF-κB activation. As examined bythe NF-κB luciferase reporter assay, we found that baicalein suppressed TNF-α-induced NF-κB activation in a dose-dependent manner. It also inhibited TNF-α-induced nuclear translocation of p65 through inhibition of phosphorylation and degradation of IκBα. Furthermore, baicalein blocked the TNF-α-induced expression of NF-κB target genes involved in anti-apoptosis (cIAP-1, cIAP-2, FLIP and BCL-2), proliferation (COX-2, cyclin D1 and c-Myc), invasion (MMP‑9), angiogenesis (VEGF) and major inflammatory cytokines (IL-8 and MCP1). The flow cytometric analysis indicated that baicalein potentiated TNF-α-induced apoptosis and induced G1 phase arrest in HeLa cells. Moreover, baicalein significantly blocked activation of p38, extracellular signal-regulated kinase 1/2 (ERK1/2). Our results imply that baicalein could be a lead compound for the modulation of inflammatory diseases as well ascertain cancers in which inhibition of NF-κB activity may be desirable. https://greenmedinfo.com/article/baicalein-could-be-lead-compound-modulation-inflammatory-diseases-well-certain#comments Baicalein Cervical Cancer Inflammation Anti-Inflammatory Agents NF-kappaB Inhibitor Tumor Necrosis Factor (TNF) Alpha Inhibitor Anti-Inflammatory Agents Baicalein Cervical Cancer Gene Expression Regulation NF-kappaB Inhibitor Tumor Necrosis Factor (TNF) Alpha Inhibitor In Vitro Study Mon, 21 Nov 2016 21:09:59 +0000 greenmedinfo 139226 at https://greenmedinfo.com Docosahexaenoic acid might influence the process of oligodendrocyte progenitor maturation. https://greenmedinfo.com/article/docosahexaenoic-acid-might-influence-process-oligodendrocyte-progenitor-matura n/a PMID:  Biochim Biophys Acta. 2017 Jun 21. Epub 2017 Jun 21. PMID: 28647405 Abstract Title:  Docosahexaenoic acid promotes oligodendrocyte differentiation via PPAR-γ signalling and prevents tumor necrosis factor-α-dependent maturational arrest. Abstract:  Docosahexaenoic acid (DHA) is an essential omega-3 fatty acid known to be neuroprotective in several models of human diseases, including multiple sclerosis. The protective effects of DHA are largely attributed to its ability to interfere with the activity of transcription factors controlling immune and inflammatory responses, including the agonist-dependent transcription factor peroxisome proliferator-activated receptor-γ (PPAR-γ). In this study, we used primary oligodendrocyte progenitor (OP) cultures from neonatal rat brain to investigate whether DHA could influence OP maturation and directly promote myelination, as previously reported for selective PPAR-γ agonists. We show that, similarly to the selective PPAR-γ agonist pioglitazone (PGZ), DHA promotes OP maturation and counteracts the maturational arrest induced by TNF-α, used to mimic inflammatory conditions. The PPAR-γ antagonist GW9662 prevented both DHA-induced OP maturation and PPAR-γ nuclear translocation, supporting the hypothesis that DHA acts through the activation of PPAR-γ. In addition, both PGZ and DHA induced the phosphorylation of extracellular signal-regulated-kinase 1-2 (ERK1/2), in a PPAR-γ-dependent manner. ERK1/2 activity is known to regulate the transition from OPs to immature oligodendrocytes and the presence of specific inhibitors of ERK1/2 phosphorylation (U0126 or PD98059) prevented the differentiating effects of both DHA and PGZ. These results indicate that DHA might influence the process of OP maturation through its PPAR-γ agonistic activity and provide novel molecular mechanisms for the action of this dietary fatty acid, further supporting the nutritional intervention in demyelinating diseases such as multiple sclerosis. https://greenmedinfo.com/article/docosahexaenoic-acid-might-influence-process-oligodendrocyte-progenitor-matura#comments Demyelinating Diseases DHA (Docosahexaenoic Acid) Multiple Sclerosis Tumor Necrosis Factor (TNF) Alpha Inhibitor Demyelinating Diseases DHA (Docosahexaenoic Acid) Multiple Sclerosis Tumor Necrosis Factor (TNF) Alpha Inhibitor In Vitro Study Mon, 26 Jun 2017 20:51:10 +0000 greenmedinfo 149611 at https://greenmedinfo.com Lactobacillus plantarum alleviates aflatoxins B1 and M1 induced disturbances in the intestinal genes expression and DNA fragmentation. https://greenmedinfo.com/article/lactobacillus-plantarum-alleviates-aflatoxins-b1-and-m1-induced-disturbances-i n/a PMID:  Toxicon. 2018 Mar 21 ;146:13-23. Epub 2018 Mar 21. PMID: 29574215 Abstract Title:  Lactobacillus plantarum alleviate aflatoxins (Band M) induced disturbances in the intestinal genes expression and DNA fragmentation in mice. Abstract:  This study aimed to assess the disturbances in intestinal genes expression and DNA fragmentation in mice treated orally with aflatoxin B(AFB) or aflatoxin M(AFM) and the protective activity of Lactobacillus plantarum (LP). Male Balb/c mice were divided into 6 groups including the control group, the group treated with 2 mg/kg b.w of LP (2 × 10 cfu/mL), the groups treated with AFBor AFM(100 μg/kg b.w), and the groups treated with AFBor AFMduring, after or before LP. Small intestines were collected for the determination of DNA fragmentation, gene expression and target protein content. The results showed that AFBor AFMincreased DNA fragmentation, down regulated the expressions of caspase-3, caspase-9, CYP3A13, Bax and p53 as well as up-regulated the expression of TNF-α and Bcl-2 and their target proteins. LP succeeded to alleviate the disturbances in DNA fragmentation and the expression of these genes. The improvement was more pronounced in the group co-administered with the toxins plus LP. It could be concluded that AFBand AFMinduced disturbances in intestinal function via the disturbances in DNA fragmentation and genes expression. LP induced a potential protective effect and is considered a promising agent against the genotoxicity induced by these mycotoxins. https://greenmedinfo.com/article/lactobacillus-plantarum-alleviates-aflatoxins-b1-and-m1-induced-disturbances-i#comments DNA damage Lactobacillus plantarum Aflatoxin Genoprotective Tumor Necrosis Factor (TNF) Alpha Inhibitor DNA damage Gene Expression Regulation Genoprotective Lactobacillus plantarum Tumor Necrosis Factor (TNF) Alpha Inhibitor Animal Study Tue, 10 Apr 2018 15:56:24 +0000 greenmedinfo 162405 at https://greenmedinfo.com Lycopene has a protective effect on non-alcoholic fatty liver disease. https://greenmedinfo.com/article/lycopene-has-protective-effect-non-alcoholic-fatty-liver-disease n/a PMID:  World J Gastroenterol. 2016 Dec 14 ;22(46):10180-10188. PMID: 28028366 Abstract Title:  Hepatoprotective and antioxidant effects of lycopene on non-alcoholic fatty liver disease in rat. Abstract:  AIM: To evaluate the hepatoprotective effect of lycopene (Ly) on non-alcoholic fatty liver disease (NAFLD) in rat. METHODS: A rat model of NAFLD was first established by feeding a high-fat diet for 14 wk. Sixty-five rats were randomly divided into normal group, model group and Ly treatment groups. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglycerides (TG), total cholesterol (TC) in serum and low density lipoprotein-cholesterol (LDL-C), high density lipoprotein-cholesterol (HDL-C), free fatty acid (FFA), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH) in liver tissue were evaluated, respectively. While the hepatoprotective effect was also confirmed by histopathological analysis, the expression levels of TNF-α and cytochrome P450 (CYP) 2E1 in rat liver were determined by immunohistochemistry analysis. RESULTS: A significant decrease was observed in the levels of serum AST (2.07-fold), ALT (2.95-fold), and the blood lipid TG (2.34-fold) and TC (1.66-fold) in the dose of 20 mg/kg Ly-treated rats (P<0.01), compared to the model group. Pretreatment with 5, 10 and 20 mg/kg of Ly significantly raised the levels of antioxidant enzyme SOD in a dose-dependent manner, to 90.95± 9.56, 109.52 ± 11.34 and 121.25 ± 10.68 (P<0.05, P<0.01), as compared with the model group. Similarly, the levels of GSH were significantly increased (P<0.05, P<0.01) after the Ly treatment. Meanwhile, pretreatment with 5, 10 and 20 mg/kg of Ly significantly reduced MDA amount by 30.87, 45.51 and 54.49% in the liver homogenates, respectively (P<0.01). The Ly treatment group showed significantly decreased levels of lipid products LDL-C (P<0.05, P<0.01), improved HDL-C level and significantly decreased content of FFA, compared to the model group (P<0.05, P<0.01). Furthermore, the Ly-treated group also exhibited a down-regulated TNF-α and CYP2E1 expression, decreased infiltration of liver fats and reversed histopathological changes, all in a dose-dependent manner (P<0.05, P<0.01). CONCLUSION: This study suggests that Ly has a protective effect on NAFLD, down-regulates expression of TNF-α, and that CYP2E1 may be one of the action mechanisms for Ly. https://greenmedinfo.com/article/lycopene-has-protective-effect-non-alcoholic-fatty-liver-disease#comments Lycopene Nonalcoholic fatty liver disease (NAFLD) Antioxidants Hepatoprotective Tumor Necrosis Factor (TNF) Alpha Inhibitor Antioxidants Dose Response Hepatoprotective lycopene Nonalcoholic fatty liver disease (NAFLD) Tumor Necrosis Factor (TNF) Alpha Inhibitor Animal Study Fri, 05 May 2017 17:41:41 +0000 greenmedinfo 147310 at https://greenmedinfo.com Puerarin prevents LPS-induced acute lung injury via inhibiting inflammatory response. https://greenmedinfo.com/article/puerarin-prevents-lps-induced-acute-lung-injury-inhibiting-inflammatory-respon n/a PMID:  Microb Pathog. 2018 Mar 20 ;118:170-176. Epub 2018 Mar 20. PMID: 29571724 Abstract Title:  Puerarin prevents LPS-induced acute lung injury via inhibiting inflammatory response. Abstract:  Acute lung injury (ALI) is a critical illness syndrome with high morbidity and mortality in patients. Inflammation has been known to be involved in the development of ALI. The purpose of this study was to investigate the effect of puerarin on lipopolysaccharide (LPS)-induced ALI in mice. The pro-inflammatory cytokines TNF-α, IL-6 and IL-1β were determined by ELISA. Western blot analysis was used for detecting the expression of NF-κB, IκBα, and LXRα. And myeloperoxidase (MPO) activity, lung wet/dry (W/D) ratio, and histopathological examination were also detected in lung tissues. The results showed that puerarinsignificantly inhibited LPS-stimulated MPO activity in lung tissues. Meanwhile, puerarin attenuated lung histopathological changes and lung wet/dry (W/D) ratio. We also found that the expression of pro-inflammatory cytokines, TNF-α, IL-6 and IL-1β were inhibited by puerarin. Puerarin also inhibited LPS-induced TNF-α in RAW264.7 cells and IL-8 in A549 cells. From the results of western blotting, puerarin significantly suppressed LPS-stimulated NF-κB activation. And the expression of LXRα was dose-dependently increased by treatment of puerarin. The inhibition of puerarin on TNF-α production in RAW264.7 cells and IL-8 production in A549 cells were blocked by LXRα inhibitor geranylgeranyl pyrophosphate (GGPP). These results suggested that puerarin attenuated ALI by activating LXRα, which subsequently inhibited LPS-induced inflammatory response. https://greenmedinfo.com/article/puerarin-prevents-lps-induced-acute-lung-injury-inhibiting-inflammatory-respon#comments Lipopolysaccharide-Induced Toxicity Lung Injury: Acute Puerarin Anti-Inflammatory Agents Tumor Necrosis Factor (TNF) Alpha Inhibitor Anti-Inflammatory Agents Lipopolysaccharide-Induced Toxicity Lung Injury: Acute Puerarin Tumor Necrosis Factor (TNF) Alpha Inhibitor In Vitro Study Wed, 16 May 2018 19:21:43 +0000 greenmedinfo 164305 at https://greenmedinfo.com Puerarin treatment may represent a novel approach to lowering the risk of or improving function in ischemia-reperfusion brain injury-related disorders. https://greenmedinfo.com/article/puerarin-treatment-may-represent-novel-approach-lowering-risk-or-improving-fun n/a PMID:  J Biomed Sci. 2009 Jan 19 ;16:9. Epub 2009 Jan 19. PMID: 19272172 Abstract Title:  Neuroprotective mechanisms of puerarin in middle cerebral artery occlusion-induced brain infarction in rats. Abstract:  Puerarin, a major isoflavonoid derived from the Chinese medical herb Radix puerariae (kudzu root), has been reported to be useful in the treatment of various cardiovascular diseases. In the present study, we examined the detailed mechanisms underlying the inhibitory effects of puerarin on inflammatory and apoptotic responses induced by middle cerebral artery occlusion (MCAO) in rats. Treatment of puerarin (25 and 50 mg/kg; intraperitoneally) 10 min before MCAO dose-dependently attenuated focal cerebral ischemia in rats. Administration of puerarin at 50 mg/kg, showed marked reduction in infarct size compared with that of control rats. MCAO-induced focal cerebral ischemia was associated with increases in hypoxia-inducible factor-1alpha (HIF-1alpha), inducible nitric oxide synthase (iNOS), and active caspase-3 protein expressions as well as the mRNA expression of tumor necrosis factor-alpha (TNF-alpha) in ischemic regions. These expressions were markedly inhibited by the treatment of puerarin (50 mg/kg). In addition, puerarin (10-50 microM) concentration-dependently inhibited respiratory bursts in human neutrophils stimulated by formyl-Met-Leu-Phe. On the other hand, puerarin (20-500 microM) did not significantly inhibit the thiobarbituric acid-reactive substance reaction in rat brain homogenates. An electron spin resonance (ESR) method was conducted on the scavenging activity of puerarin on the free radicals formed. Puerarin (200 and 500 microM) did not reduce the ESR signal intensity of hydroxyl radical formation. In conclusion, we demonstrate that puerarin is a potent neuroprotective agent on MCAO-induced focal cerebral ischemia in vivo. This effect may be mediated, at least in part, by the inhibition of both HIF-1alpha and TNF-alpha activation, followed by the inhibition of inflammatory responses (i.e., iNOS expression), apoptosis formation (active caspase-3), and neutrophil activation, resulting in a reduction in the infarct volume in ischemia-reperfusion brain injury. Thus, puerarin treatment may represent a novel approach to lowering the risk of or improving function in ischemia-reperfusion brain injury-related disorders. https://greenmedinfo.com/article/puerarin-treatment-may-represent-novel-approach-lowering-risk-or-improving-fun#comments Brain Ischemia Middle Cerebral Artery Occlusion (MCAO) Puerarin Antioxidants Neuroprotective Agents Tumor Necrosis Factor (TNF) Alpha Inhibitor Vasodilator Agents Antioxidants Brain Ischemia Middle Cerebral Artery Occlusion (MCAO) Neuroprotective Agents Tumor Necrosis Factor (TNF) Alpha Inhibitor Vasodilator Agents Animal Study Wed, 06 Jun 2018 23:38:22 +0000 greenmedinfo 165389 at https://greenmedinfo.com