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  1. Dahmardeh N, Shabani M, Basiri M, Kalantaripour TP, Asadi-Shekaari M
    Malays J Med Sci, 2019 Jul;26(4):28-38.
    PMID: 31496891 DOI: 10.21315/mjms2019.26.4.4
    Background: There is a meaningful necessity for a targeted therapy of essential tremor (ET), as medications have not been developed specifically for ET. For nearly a century, many drugs have been applied in the treatment of tremor but the drug treatment of ET remains still unknown. Some potential therapeutic factors such fingolimod (FTY720) can be effectively used to treat ET in animals. In the present research, the effect of FTY720, the immunomodulatory sphingosine 1-phosphate (S1P) analog, on degeneration of cerebellar and olivary neurons induced by harmaline in male rats was investigated.

    Methods: The animals were allotted into control dimethyl sulfoxide (DMSO), saline + harmaline [30 mg/kg, intraperitoneally, (i.p.)], harmaline + FTY720 (1 mg/kg, i.p, 1 h and 24 h before harmaline injection) groups (n = 10). The cerebellum and inferior olive nucleus (ION) were studied for neuronal degeneration using immunohistochemistry (IHC) and ultrastructural study by transmission electron microscopy (TEM) techniques.

    Results: Harmaline caused neuronal cell loss, caspase-3 mediated apoptosis, astrocytosis and ultrastructural changes in cerebellar Purkinje cells and inferior olive neurons. FTY720 exhibited neuroprotective effects on cerebellar Purkinje cells and inferior olivary neurons.

    Conclusion: These results suggest that FTY720 has potential efficacy for prevention of ET neurodegeneration and astrocytosis induced by harmaline in male rats.

  2. Zamiri R, Abbastabar Ahangar H, Zakaria A, Zamiri G, Shabani M, Singh B, et al.
    Chem Cent J, 2015;9:28.
    PMID: 26089982 DOI: 10.1186/s13065-015-0099-y
    In this paper a template-free precipitation method was used as an easy and low cost way to synthesize Ag2S semiconductor nanoparticles. The Kramers-Kronig method (K-K) and classical dispersion theory was applied to calculate the optical constants of the prepared samples, such as the reflective index n(ω) and dielectric constant ε(ω) in Far-infrared regime.
  3. Abdi M, Pasbakhsh P, Shabani M, Nekoonam S, Sadeghi A, Fathi F, et al.
    Neurotox Res, 2021 Dec;39(6):1732-1746.
    PMID: 34570348 DOI: 10.1007/s12640-021-00417-y
    Multiple sclerosis (MS) is a chronic disorder characterized by reactive gliosis, inflammation, and demyelination. Microglia plays a crucial role in the pathogenesis of MS and has the dynamic plasticity to polarize between pro-inflammatory (M1) and anti-inflammatory (M2) phenotypes. Metformin, a glucose-lowering drug, attenuates inflammatory responses by activating adenosine monophosphate protein kinase (AMPK) which suppresses nuclear factor kappa B (NF-κB). In this study, we indirectly investigated whether metformin therapy would regulate microglia activity in the cuprizone (CPZ)-induced demyelination mouse model of MS via measuring the markers associated with pro- and anti-inflammatory microglia. Evaluation of myelin by luxol fast blue staining revealed that metformin treatment (CPZ + Met) diminished demyelination, in comparison to CPZ mice. In addition, metformin therapy significantly alleviated reactive microgliosis and astrogliosis in the corpus callosum, as measured by Iba-1 and GFAP staining. Moreover, metformin treatment significantly downregulated the expression of pro-inflammatory associated genes (iNOS, H2-Aa, and TNF-α) in the corpus callosum, whereas expression of anti-inflammatory markers (Arg1, Mrc1, and IL10) was not promoted, compared to CPZ mice. Furthermore, protein levels of iNOS (pro-inflammatory marker) were significantly decreased in the metformin group, while those of Trem2 (anti-inflammatory marker) were increased. In addition, metformin significantly increased AMPK activation in CPZ mice. Finally, metformin administration significantly reduced the activation level of NF-κB in CPZ mice. In summary, our data revealed that metformin attenuated pro-inflammatory microglia markers through suppressing NF-κB activity. The positive effects of metformin on microglia and remyelination suggest that it could be used as a promising candidate to lessen the incidence of inflammatory neurodegenerative diseases such as MS.
  4. Jabbari M, Barati M, Shabani M, Kazemian E, Khalili-Moghadam S, Javanmardi F, et al.
    Nutr Cancer, 2022 Jan 20.
    PMID: 35048753 DOI: 10.1080/01635581.2021.2009884
    Bioactive peptides (BPs) content of dairy products is suggested to be a significant ingredient for reducing breast cancer (BC) risk. There is no observational study regarding the correlation between BPs and the risk of chronic disease because BPs' content of food items has not been evaluated in any study. The goal of the current study was to assess the association of dairy-originated BPs with BC risk. One hundred thirty-four women with BC and 267 cancer-free controls were selected from referral hospitals in Tehran, Iran. The development of an in-silico model for estimation of the bioactive and digestion-resistant peptides content of dairy products was done in our previous research. The risk assessment for BPs and BC association was performed across the tertiles of the peptide's intake. Odds ratios (OR) were calculated by logistic regression. The negative association of all bioactive and digestion-resistant peptides except for peptides with high hydrophilicity and low bioactivity was seen in all models. In PR-negative subjects only the association of total dairy intake (OR: 0.61; 95% CI: 0.26-1.45; P for trend: 0.276), peptides with low bioactivity (OR: 0.40; 95% CI: 0.16-1.02; P for trend: 0.0.052), antidiabetic peptides (OR: 0.42; 95% CI: 0.17-1.05; P for trend: 0.0.062) and di-peptides (OR: 0.42; 95% CI: 0.17-1.05; P for trend: 0.0.062) were not significant in the final model. Also, no significant association between ER-negative subjects and total dairy intake (OR: 0.41; 95% CI: 0.16-1.07; P for trend: 0.0.068) was noted. Our findings deduced that milk-derived BPs negatively associate with the risk of ER/PR/HER2 negative BC among Iranian women.Supplemental data for this article is available online at https://doi.org/10.1080/01635581.2021.2009884.
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