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           Search results for: Rat Tumor Necrosis Factor alpha TNF-α   

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#28933980   2017/09/21 Save this To Up

Panduratin A Prevents Tumor Necrosis Factor-Alpha-Induced Muscle Atrophy in L6 Rat Skeletal Muscle Cells.

Panduratin A, a prenylated chalcone compound, has anti-obesity, anti-bacterial, anti-cancer, anti-inflammatory, and anti-oxidative activities. However, its preventive effect on muscle atrophy has not been studied. The purpose of this study was to evaluate the inhibitory effect of panduratin A on muscle atrophy and to investigate its molecular mechanisms in tumor necrosis factor-alpha (TNF-α)-treated L6 rat skeletal muscle cells. Panduratin A restored the myotube diameter reduced by TNF-α. At the molecular level, panduratin A elevated phosphatidylinositol 3 kinase/Akt/mammalian target of rapamycin pathway and stimulated the MyoD and myogenin mRNA expression decreased by TNF-α. However, panduratin A attenuated the mRNA expression of E3 ubiquitin ligase and autophagy-related genes. Moreover, panduratin A significantly inhibited reactive oxygen species production by increasing the mRNA expression of catalase and superoxide dismutase. Overall, panduratin A might be a useful agent for the treatment of muscle atrophy.

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#28933311   2017/09/21 Save this To Up

MG17, a novel triazole derivative abrogated neuroinflammation and related neurodegenerative symptoms in rodents.

The objective of present study is to explore multiple effects of the compound MG17 and relate them to achieve better therapeutic potential against neuroinflammation related disorders. We examined whether our compound is acting through regulating neuroinflammatory mediators. We have done some preliminary behavioral studies to shortlist the derivatives using rodent models of peripheral nerve injury in our earlier publication and now we extended our screening studies to explore the test compounds efficacy on other related peripheral neurological disorders such as Streptozotocin-induced diabetic peripheral neuropathy (DPN) and methyl mercury (MeHg) induced neurodegeneration in rats. Pro-inflammatory cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were quantified with RT-qPCR studies and histopathology studies were performed taking tissue samples from MeHg induced neurodegeneration rats. The effect of MG17 was assessed on local and acute inflammation through carrageenan-induced rat paw edema model. We observed the reduction in nociceptive responses in DPN rats. Pain threshold was reduced greater than 50% in various pain assessment modules. Upregulated pro-inflammatory cytokines which are thought to have a prominent role in neuroinflammation was controlled near to normal level quantified by RT-PCR studies. However, MG17 was able to regulate IL-6 and TNF-α but not IL-1β. Our results clearly suggest the beneficial potential of compound MG17 through inhibition of pro-inflammatory cytokines upregulation. MG17 could be an intriguing therapeutic approach in diabetes-related neuro-pathophysiological conditions.

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#28931778   2017/09/21 Save this To Up

The anti-inflammatory pathway regulated via nicotinic acetylcholine receptors in rat intestinal mesothelial cells.

Regulation of inflammation in intestinal mesothelial cells in the abdominal cavity is important for the pathogeny of clinical conditions, such as postoperative ileus, peritonitis and encapsulating peritoneal sclerosis. Here we have examined the inflammatory effect of lipopolysaccharide (LPS) and the anti-inflammatory effect of nicotinic acetylcholine receptor stimulation in rat intestinal mesothelial cells. LPS upregulated mRNA expression of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), monocyte chemotactic protein-1 (MCP-1) and inducible nitric oxide synthase (iNOS). The α7, α9 and α10 subunits of nicotinic acetylcholine receptor were detected in intestinal mesothelial cells. Nicotine (10 nM) significantly inhibited LPS-induced mRNA expression of IL-1β and iNOS, but not TNF-α and MCP-1. In addition, the α7 nicotinic acetylcholine receptor selective agonist, PNU-282987 (10 nM), significantly inhibited LPS-induced mRNA expression of IL-1β but not TNF-α, iNOS and MCP-1. Finally, we found that enteric nerves adhered to intestinal mesothelial cells located under the ileal serosa. In conclusion, intestinal mesothelial cells react to LPS to induce the production of nitric oxide from iNOS. The anti-inflammatory action of intestinal mesothelial cells expressing α7nAChR may be mediated via their connectivity with enteric nerves.

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#28927460   2017/09/20 Save this To Up

Protective effect of hydrogen-saturated saline on acute lung injury induced by oleic acid in rats.

The purpose of the study is to investigate the role and mechanisms of hydrogen-saturated saline (HSS) in the acute lung injury (ALI) induced by oleic acid (OA) in rats.

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#28925127   2017/09/19 Save this To Up

[Mechanism of Rhei Radix et Rhizoma combined with Scutellariae Radix on liver inflammation in rats with endotoxin disease based on p38MAPK pathway].

To explore the mechanism of Rhei Radix et Rhizoma combined with Scutellariae Radix in regulatory lipopolysaccharide (LPS)-induced liver inflammation in rats with endotoxin blood, 50 male SD rats were selected and randomly divided into blank group, model group, dexamethasone group, herbal pair high dose group, herbal pair low dose group, with 10 in each group. Rats in each were given preventive drugs for 7 consecutive days. At 0.5 h after the final administration, the model was built through the tail vein injection with LPS (5 mg•kg⁻¹). Then, animal anal temperatures were determined and recorded once every 0.5 h. The rats were killed at 4 h after the modeling to determine spleen thymus coefficient. ELISA method was used to detect cytokines interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α) in liver tissues. The colorimetric method was applied in determination of oxidation nitrogen (NO) content in liver tissues. Western Blot method was adopted to detect Toll-like receptor protein 4, p38MAPK p38MAPK, phosphorylated p38MAPK (p-p38MAPK) and nitric oxide synthase (iNOS) protein expressions. The results showed that compared with the blank group, in the model group, TLR4 protein expression, iNOS protein expression and p38 phosphorylation expression, IL-1β, NO and TNF-α content increased significantly in liver tissues (P<0.05 or P<0.01). And compared with the model group, the herbal pair high dose group showed significantly reduction in IL-1β, NO and TNF-α expressions in rat liver tissues (P<0.05 or P<0.01), down-regulation in iNOS protein expression and p38 phosphorylation expression in rat liver tissues (P<0.05), but without significant up-regulation in TLR4 protein. Low-dose herbal pair can significantly reduce IL-1β and NO expression in model rat liver tissues (P<0.01), significantly down-regulate iNOS protein expression (P<0.01), with a slight down-regulation in phosphorylation of p38 but no statistical significance, and no reduction in TLR4 expression. In conclusion, the compatibility of Rhei Radix et Rhizoma combined with Scutellariae Radix may reduce the expression of iNOS protein and the release of inflammatory cytokines IL-1β, NO and TNF-α by decreasing p38 protein phosphorylation expression and blocking p38MAPK signaling pathways, so as to alleviate the inflammation reaction and protect the liver.

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#28923326   2017/09/19 Save this To Up

Effects of Sulphasalazine in Cerebral Ischemia Reperfusion Injury in Rat.

Management of cerebral ischemia/reperfusion (I/R) injury is still difficult process today.

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#28923114   2017/09/19 Save this To Up

Homocysteine exaggerates microglia activation and neuroinflammation through microglia localized STAT3 overactivation following ischemic stroke.

Elevated plasma homocysteine (Hcy) levels have been indicated as a strong and modifiable risk factor of ischemic stroke; the previous studies have shown that exposure to Hcy activates cultured microglia. However, whether neurotoxicity of Hcy involves microglia activation following brain ischemia and the underlying mechanisms remains incompletely understood.

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#28917082   2017/09/16 Save this To Up

Protective effect of salusin-α and salusin-β against ethanol-induced gastric ulcer in rats.

Alcohol consumption has been found to be associated with gastric ulcers, including gastric mucosal lesions. Salusin-α and salusin-β are bioactive peptides having 28 and 20 amino acids, respectively. Salusin-α and salusin-β immunoreactivity has been detected in the stomach and in the intestines. It has been reported that the salusins regulate the cytokine levels and decrease the infarct area in the heart tissue after ischemia. In this study, we investigated the effects of the salusins in the gastric injury formed with ethanol.

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#28915567   2017/09/16 Save this To Up

Melatonin inhibits Sirt1-dependent NAMPT and NFAT5 signaling in chondrocytes to attenuate osteoarthritis.

Osteoarthritis (OA) is a degenerative joint disease mainly characterized by cartilage degradation. Interleukin-1β (IL-1β) contributes to OA pathogenesis by enhancing oxidative stress and inflammation. Melatonin reportedly elicits potent protection against OA. However, the role of melatonin and underlying mechanism in IL-1β-stimulated chondrocytes remain largely unclear. In this study, we found that melatonin inhibited IL-1β-induced toxicity and sirtuin 1 (Sirt1) enhancement in human chondrocytes. Melatonin reduced the IL-1β-increased nicotinamide phosphoribosyltransferase (NAMPT) expression and the NAD(+) level in chondrocytes in a Sirt1-dependent manner. In turn, the inhibitory effect of melatonin on Sirt1 was mediated by NAMPT. Moreover, melatonin suppressed IL-1β-induced Sirt1-mediated matrix metalloproteinase (MMP)-3 and MMP-13 production. Melatonin also decreased the Sirt1-steered nuclear factor of activated T cells 5 (NFAT5) expression in IL-1β-challenged chondrocytes. NFAT5 depletion mimicked the suppressive effects of melatonin on IL-1β-elevated production of inflammatory mediators, including tumor necrosis factor-α (TNF-α), IL-1β, prostaglandin E2 (PGE2), and nitric oxide (NO) in chondrocytes. TNF-α, IL-1β, PGE2, or NO decrease caused the similar reduction of MMP-3 and MMP-13 by melatonin in IL-1β-insulted chondrocytes. Highly consistent with in vitro findings, in vivo results demonstrated that melatonin repressed the expression of relevant genes in rat OA pathogenesis in anterior cruciate ligament transection model. Overall, these results indicate that melatonin effectively reduced IL-1β-induced MMP production by inhibiting Sirt1-dependent NAMPT and NFAT5 signaling in chondrocytes, suggesting melatonin as a potential therapeutic alternative for chondroprotection of OA patients.

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#28915536   2017/09/16 Save this To Up

Protective effect of the standardized extract of ginkgo biloba (EGb761) against hypertension with hypercholesterolemia-induced renal injury in rats: Insights in the underlying mechanisms.

The potential protective role of the standardized leaf extract of ginkgo biloba (EGb761) on hypertension with hypercholesterolemia-induced renal injury was investigated in rats. Hypertension was induced by L-N(G)-nitroarginine methyl ester (L-NAME) and hypercholesterolemia was induced by feeding rats with a diet containing 1% cholesterol. In these animals repeated treatment with EGb761 produced a progressive reduction in the systolic, diastolic and mean arterial blood pressure (BP). EGb761 increased the progressive reduction in the systolic, diastolic and mean arterial BP induced by repeated administration of losartan with simvastatin. EGb761 corrected the compromised serum lipid profile and enhanced the effect of losartan with simvastatin on lipid profile. EGb761 protected against hypertension with hypercholesterolemia-induced renal injury as assessed by measurement of serum renal function markers and by histopathological examination. EGb761 enhanced the renoprotective effect of losartan with simvastatin in these rats. Concomitantly, hypertension with hypercholesterolemia-induced elevation of renal tissue malondialdehyde (MDA) and nitrite levels and reduction of intracellular reduced glutathione (GSH) level were inhibited by repeated treatment with EGb761. In addition, hypertension with hypercholesterolemia-induced increases in tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) levels in renal tissues were inhibited by treatment with EGb761. Also, EGb761 inhibited hypertension with hypercholesterolemia-induced decrease in endothelial nitric oxide synthase (eNOS) protein expression and increase in the protein expressions of inducible NO synthase (iNOS), TNF-α, IL-6 and IL-1β in the kidney tissues. Losartan with simvastatin produced similar effects on renal tissues oxidative stress, nitrite and inflammatory markers levels and on protein expressions of eNOS, iNOS, TNF-α, IL-6 and IL-1β. EGb761 enhanced losartan with simvastatin effects. These results indicate that EGb761 has the ability to protect against hypertension with hypercholesterolemia-induced renal injury. The ability of EGb761 to provide this renoprotective effect may positively correlate, besides its antihypertensive and antihypercholesterolemic effects, to its ability to suppress renal oxidative stress, nitrosative stress and inflammation.

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