13 research outputs found

    The Contribution of S100B Suppression by Arundic Acid to the Inhibition of the Glio-Toxicity Induced by Beta-Amyloid in an Astrocytes Culture

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    Background & Objective: It has been shown that glial activation has important role in the pathophysiology of Alzheimer’s disease. S100B is an astrocyte specific factor with deleterious effects on the neuronal and non-neuronal cells in the central nervous system. Arundic acid is an agent that inhibits the secretion and production of S100B in astrocytes. Therefore, we aimed to evaluate the contribution of S100B in the cyto-protective effects of Arundic acid against beta-amyloid in 1321N1 astrocyte cell culture. Materials & Methods: Human astrocyte cells (1321N1) were treated with beta-amyloid (200 μM) and / or Arundic acid (50 μM) for 24 hours. Cell viability was measured using the MTT (3, 4, 5-dimethylthiazole-2, 5-diphenyl tetrazolium bromide) method. The S100B protein level was measured by the ELISA method. Results: Beta-amyloid treatment reduced cell survival compared to the control-treated groups. In contrast, the addition of Arundic acid to beta-amyloid suppressed the beta-amyloid-induced cell death. Beta-amyloid also increased the S100B protein level. However, Arundic acid prevented the rise of S100B protein level induced by beta-amyloid. Conclusion: The reduction of S100B protein secretion may be involved in the protective effects of Arundic acid against the beta-amyloid induced Glio-toxicity in the astrocyte culture

    Association of CD1A+ 622 T/C,+ 737 G/C and CD1E+ 6129 A/G Genes Polymorphisms with Multiple Sclerosis

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    Antibodies and specific T cells to glycolipids have been found in MS patients. CD1 molecules are involved in presentation of lipid antigens to T-cells. Therefore, functional polymorphisms in two CD1 genes (+ 622 T/C and+ 737 G/C in CD1A along with+ 6129 A/G in CD1E) might be associated with susceptibility to MS. First, 351 MS patients and 342 controls were enrolled in this study. Allele-specific oligonucleotide polymerase chain reaction and PCR-RFLP methods were used for genotyping. The frequency of CD1A

    EFFECTS OF TEUCRIUM POLIUM ON ORAL GLUCOSE TOLERANCE TEST, REGENERATION OF PANCREATIC ISLETS AND ACTIVITY OF HEPATIC GLUCOKINASE IN DIABETIC RATS

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    Background and Objective – Hepatotoxicity associated with the hypoglycemic effects of an aqueous extract of Teucrium polium was previously described. In this investigation, the effects of the extract on oral glucose tolerance test, regeneration of pancreatic islets and hepatic glucokinase activity of streptozocin-induced diabetic rats were studied. Methods – An aqueous extract of T. polium was fed by gavage tube to healthy and streptozocin-induced diabetic rats for several days. Oral glucose tolerance, number of pancreatic islets and hepatic glucokinase activity were measured using standard methods and compared between diabetic and healthy rats. Results – In diabetic animals, the aqueous extract caused a significant reduction (p < 0.001) in the level of serum glucose during oral glucose tolerance tests. The number of pancreatic islets per unit area significantly increased (p < 0.01) and glucokinase activity was significantly elevated (p < 0.01) in diabetic animals treated with the extract. Conclusion – Although aqueous extract of T. polium contains some hepatotoxic compounds, it also contains components that are beneficial in the treatment of streptozocin-induced diabetes

    Protective Effects of Vitamin E and/or Quercetin Co-Supplementation on the Morphology of Kidney in Cyclosporine A-Treated Rats

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    Background: Cyclosporine A (CsA) is a nephrotoxic immunosuppressivedrug. Antioxidants might attenuate its toxicity. Inthe present study, the effects of vitamin E and quercetin on themorphology of kidney in CsA-treated rats were investigated.Methods: Six groups of rats were used in this gavage feedingstudy either for 4 or 8 weeks. Groups 1 and 2 received eitherolive oil or 25% ethanol in olive oil per day. Group 3 receivedCsA (25 mg/kg/day) in olive oil. All other groups received CsAplus the following: group 4, vitamin E (100 mg/kg/day) in oliveoil; group 5, quercetin (15 mg/kg/day) in 25% ethanol in oliveoil; and group 6, vitamin E plus quercetin. In the final day of thestudy, the animals were sacrificed and kidney sections were preparedfor morphologic studies using light microscopy.Results: Acute morphologic alterations induced by CsA in thekidney tubules included isometric vacuolization, brush borderloss, microcalcification, and presence of inclusion bodies. Smoothmuscle degeneration and necrosis were developed in arterioles.Treatment with vitamin E plus quercetin prevented severe,moderate, and mild abnormalities of the tubules. However fibrosiswas the only microscopic change of the interstitium thatwas not present in animals treated with vitamin E plusquercetin after both periods.Some mild morphological changes of the blood vesselssuch as arteriolar medial smooth muscle degeneration and necrosis,arteriolar myocyte dropout and arteriolar wall hyalinizationcaused by CsA disappeared with administration of vitaminE, quercetin or vitamin E plus quercetin in both periods.Conclusion: Co-administration of vitamin E plus quercetinwith CsA in renal transplant patients may be beneficial inreducing the nephrotoxic effects of CsA

    The association between PD-1 gene polymorphisms and susceptibility to multiple sclerosis

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    AbstractProgrammed cell death 1 (PD-1) is an immune checkpoint and has been reported to be associated with several autoimmune diseases. We aimed to investigate the association between human PD-1 gene (PDCD1) polymorphisms and multiple sclerosis (MS). This case-control study was conducted on 229 MS patients and 246 healthy controls. Genotyping of rs36084323 (PD-1.1 G/A), rs11568821 (PD-1.3 G/A) and rs2227981 (PD-1.5 C/T) polymorphisms was performed by PCR-RFLP technique. The frequency difference of PD-1.1 genotypes and alleles (−536 G/A) between patients and healthy controls was not significant. Regarding PD-1.3, the AA + AG genotype was found to be relatively higher in the control group. Concerning PD-1.5 (+7785 C/T), the frequency of T allele carriers (TT + CT) was relatively higher in MS patients, which was marginally insignificant (p = .07). PD-1 gene polymorphisms may be associated with MS; however, accurate conclusions require further studies with a larger number of samples

    AT1R A1166C variants in patients with type 2 diabetes mellitus and diabetic nephropathy

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    Background: There are inconsistent reports related to the role of angiotensin II type 1 receptor (AT1R) on the risk of type 2 diabetes mellitus (T2DM) and its renal complications. Objectives: To identify the association between AT1R A1166C variants with the risk of T2DM and also with diabetic nephropathy (DN). Patients and Methods: In a case-control study, the AT1R A1166C polymorphism was detected in 135 T2DM patients with and without DN and in 98 healthy subjects from Western Iran. The genotypes of AT1R A1166C polymorphism were detected using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Results: The frequencies of AT1R A1166C genotypes and alleles were not significantly difference between patients with and without DN and controls. The frequencies of rare allele of 1166 C were 10%, 16.5%, 15.9% and 15.3% in micro-, macro- and normo-albuminuric patients and in healthy individuals, respectively (P > 0.05). The systolic blood pressure and serum creatinine level in DN patients were significantly higher in carriers of AT1R CC compared to carriers of AT1R AA genotype. In the presence of uncontrolled hyperglycemia (HbA1c > 7.5%), there was a trend toward increased risk of macro-albuminuria in carriers of AC+CC genotype (OR=3.66, [95% CI: 0.81-16.58], P = 0.092). Conclusions: Our study indicated the absence of an association between AT1R A1166C polymorphism with the risk of T2DM and DN. It seems in carriers of AT1R C allele systolic blood pressure and serum creatinine level to be higher compared to the A allele carriers
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