solaleh emamgholipour

A great interest for determining the particular mechanisms underlying lipogenesis and adipogenesis has been raised among researchers in order to fight obesity. We aimed to investigate the gene expression of FAS and its role in regulation of lipogenesis and adipogenesis in visceral adipose tissues from obese and normal-weight subjects.

A total of.participants including 40 obese patients(BMI≥35 kg/m2 according to WHO criteria) and 20 healthy subjects(BMI=18.8-24.9 kg/m2 according to WHO criteria) were recruited from who were referred to Erfan, Loghman Hakim, Sina, and Imam Khomeini hospitals bypass or sleeve gastrectomy surgeries in obese ones and elective surgery in controls. Participants were all woman aged from 20-50 years and postmenopausal subjects were not included in this study. Isolated total RNA from adipose tissue was used to synthesize complementary DNA(cDNA) and quantitative real-time PCR was performed for analyzing the gene expression of FAS, and ACC. Data was normalized to geometric means of GAPDH and β-actin expression levels.

in VAT from obese subjects, gene expression of FAS was higher than in those from controls. We found a positive correlation between genes expression of FAS and ACC with obesity indices.

It appears that obesity is associated with dysregulation of FAS genes involved in lipogenesis and adpogenesis.

Several studies suggested that beta-actin, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and 18S rRNA are expressed constitutively and contribute to the fundamental reference actions essential for cell viability and maintenance. However, there are inconsistency in this regard. Hence, we aimed to evaluate the accuracy of these three potential reference genes for Real‐Time quantitative reverse transcriptase‐polymerase chain reaction (qRT‐PCR) application for normalization in two types of human adipose tissues.

Subcutaneous and visceral fat tissues were derived from 19 healthy and 20 obese subjects and RT-qPCR was applied to determine the expression levels of beta-actin, GAPDH, and18S rRNA.

The gene expression level of beta-actin, GAPDH, and 18S rRNA was essentially the same in the subcutaneous and visceral fat tissues of all participants (P>0.05). Hence, all considered housekeeping genes displayed high expression stability and the analysis revealed that normalization to all of these three housekeeping genes gave a result that satisfactorily reflected the acceptable mRNA expression levels in adipose tissues.

Collectively, our findings suggest of beta-actin, GAPDH, and18S rRNA as reference genes applicable in human adipose tissue in the context of obesity.

Obesity with a rapid grow in developed and developing countries has a close association with higher disposition to related diseases such as hypertension. Intracellular functions of sodium, potassium, calcium, phosphate, and iron have been an interested subject in obese patients since their dysregulations are linked to a higher risk of hypertension and other metabolic disorders.

In this study, the circulating levels of sodium, potassium, calcium, phosphate, and iron were determined in the serum of obese patients compared to normal-weight people. Moreover, we examined the correlation of such electrolytes with the well-known indices of obesity such as body mass index (BMI), waist circumference (WC), hip, triglycerides (TG), cholesterol and other characterizations.

The mean levels of sodium, potassium, calcium, phosphate, and iron were significantly different (p < 0.05) in obese patients compared to normal-weight subjects. We observed a positive partial correlation between the levels of these electrolytes and obesity indices such as BMI, WC, hip, and cholesterol.

Collectively, the present study suggests the positive correlation between obesity and the indices of metabolic disorders such as hypertension and renal failure according to the observed imbalances in the concentration of electrolytes. Moreover, efforts for diet modification may be helpful in the programs aimed at decreasing the burden of obesity and related disorders.

We aimed to determine the effect of lavandula angustifolia essential oil (LEO) on IL-23 and brain-derived neurotrophic factor (BDNF) gene expressions in peripheral blood mononuclear cells (PBMCs) of relapse-remitting MS (RRMS) patients.
LEO was prepared using the hydrodistilation method on the plants aerial parts. 8 female RRMS patients and 8 healthy sex and age matched controls were entered into this study. PBMC cells were separated using Ficoll method and were treated with a concentration of 225 µg/ml LEO which and then the mRNAs were used for determining the effects of LEO on IL-23 and BDNF gene expressions using Quantitative Real Time PCR technique. Moreover in order to determine the anti-inflammatory effects of LEO, we measured the gene expression of IL-6 and IL-23 in stimulated healthy PBMC cells treated with LEO.
Results showed that there is no significant difference between PBMC of patients compared to healthy controls in case of IL-23 gene expression. Moreover, LEO has no significant effect on gene expression of IL-23 in PBMC of neither patients nor control. Also the results showed that BDNF gene expression is reduced to 41% compared to healthy controls and LEO can increase the BDNF gene expression by 81% in patients PBMCs. Moreover we observed that LEO can significantly reduce the LPS stimulated IL-6 gene expression in healthy PBMCs but had no significant effect on IL-23 gene expression.
The present study demonstrated that L.angustifolia essential oil may have a protective effect against neuron damage via increasing the gene expression of BDNF in PBMCs from RRMS patients. However, further studies are necessary to confirm our results.

Recently, much attention has been directed towards considering activated microgelial cells as putative targets for treatment of neurological disorders. MigriHeal® as a novel herbal remedy was introduced for the treatment of migraine headaches. The previous researches has shown that MigriHeal® extracts can decrease NO in an in vitro inflammatory model. The aim of this study was to investigate the effect of MigriHeal® on NO generation from LPS- stimulated microglia cells.
Neonatal rat primary microglial cells were isolated from the mixed glial cultures and the purity of the cultures was determined by immunocytochemistry. Microglial cells were pretreated with Migri-Heal® and activated by 1μg/ml LPS. Subsequently, NO levels in the culture supernatants were measured by a griess reaction. Our results showed that Migri-Heal® 50μg/ml significantly reduced NO level in inflamed microglia in a dose-dependent manner.
The results showed that different concentrations of Migri-Heal® had no prominent effect on cell viability in presence of LPS as compared with the control group. In addition, the pretreatment of microglia cells with Migri-Heal® can prevent from a morphological changes of the cells into the round and phagocytic shape.
Our study demonstrated that MigriHeal® might have NO scavenging properties. Integrative studies are warranted to uncover the novel pharmacological insights of this herbal remedy as an putative therapeutic approach against diseases - associated with inflammation.

Little in known regarding the clinical relevance of SIRT1 in multiple sclerosis (MS). Here, we aimed to evaluate mRNA expression, protein level and enzyme activity of SIRT1 in peripheral blood mononuclear cells (PBMCs) isolated from relapsing –remitting MS patients (RRMS) and healthy controls.
Twenty patients with RR-MS and twenty two age- and sex-matched healthy subjects were enrolled in this case-control study. Following PBMCs isolation, mRNA expression was evaluated by real time-PCR. SIRT1 activity and SIRT1 protein level were measured using a fluorometric assay and an enzyme-linked immunosorbent assay (ELISA) respectively, in PBMC lysates.
There was no statistically significant difference in the mRNA expression of SIRT1 (p=0.56) and its protein levels (p=0.15) between MS patients and healthy subjects. By contrast, SIRT1 enzyme activity were significantly (p=0.008) lower in RRMS patients compared with that in healthy subjects.
Our findings demonstrated that enzyme activity of SIRT1 is significantly lower in PBMCs of RRMS patients in comparison with healthy subjects. However, more investigations are essential to clarify the role of SIRT1 in MS pathogenesis.

The neuropeptide calcitonin gene-related peptide (CGRP) has long been postulated to play an integral role in the pathophysiology of migraine. Earlier studies showed that CGRP can stimulate the synthesis and release of nitric oxide (NO) and cytokines from trigeminal ganglion glial cells. The purpose of this study was to determine the effect of 17β-estradiol in regulation of CGRP expression, inducible nitric oxide synthase (iNOS) activity, and NO and interleukin-1beta (IL-1β) release in cultured peripheral blood mononuclear cells (PBMCs) from patients with pure menstrual migraine and healthy individuals. This study was performed on twelve patients with pure menstrual migraine and twelve age-and sex-matched healthy individuals. PBMCs treated with 17β-estradiol for 24 hr at physiological and pharmacological doses. Gene expression was evaluated by real time-PCR. CGRP and IL-1β proteins in culture supernatant were determined by ELISA method. Activity of iNOS in PBMCs and total nitrite in the culture supernatant were measured by colorimetric assays. Treatment with 17β-estradiol had a biphasic effect on expression of CGRP. We found that 17β-estradiol treatment at pharmacological dose significantly increases mRNA expression of CGRP in both groups (P<0.001), whereas at physiological dose it could significantly decrease CGRP mRNA expression (P<0.001), CGRP protein levels, IL-1β release, NO production and iNOS activity only in patient groups (P<0.05). Collectively, it appears that 17β-estradiol can exert protective effect on decrease of inflammation in migraine via decrease in levels of CGRP, IL-1β and iNOS activity; however, more studies are necessary in this regard.

It is evident that oxidative stress plays a crucial role in etiology of multiple sclerosis (MS). Dysregulation of antioxidant enzymes have been implicated in demylination and neuronal loss in MS. The aim of this study was to evaluate mRNA expression and activity of manganese superoxide dismutase (MnSOD), and catalase in peripheral blood mononuclear cells (PBMCs) from patients with relapsing-remitting multiple sclerosis (RRMS) and healthy controls.

We recruited 20 RRMS patients and 20 age-and sex-matched healthy subjects. PBMCs were isolated, RNA was extracted and real time-PCR was used to evaluate mRNA expression of MnSOD and catalase. Enzyme activity of MnSOD and catalase were measured using colorimetric assays.

We found a significant increase in mRNA expression and activity of catalase in PBMCs from patients compared with controls, which was accompanied by reduced activity and expression of MnSOD in MS patients.

It appears that impaired antioxidant enzymes in term of high activity of catalase and decreased activity of MnSOD are involved in MS pathogenesis, however further studies are needed to establish this concept.