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Showing 6 results for Mansouri

Firouzeh Gholampour, Sareh Mansouri,
Volume 0, Issue 0 (7-2019)
Abstract

Background: Renal ischemia/reperfusion (IR) is considered as one of the most prevalent reasons of acute renal failure (ARF). As renal failure is progressed, renal gluconeogenesis and insulin clearance are decreased. Berberine is the most important alkaloid of Berberis vulgaris. It has anti-diabetic, anti-inflammatory, and anti-microbial properties. The goal of this study was to assign the effect of RIR on the pancreas and to define the effect of berberine on the pancreatic damages induced by RIR. Methods: Male rats were allocated into four groups (n=7): Sham (no intervention), Ber (Berberine, 15 mg/kg/day), I/R (subjected to 45 min bilateral renal artery occlusion), Ber + I/R (Berberine, 15 mg/kg/day). After 24 hr, blood samples were gathered for biochemical analysis, and eventually pancreas tissue samples were kept for subsequent histological examination. Results: The ischemic challenge of kidneys resulted in pancreatic vascular congestion, which was associated with decreased plasma level of glucose as well as increased plasma insulin, creatinine, and blood urea nitrogen levels at the termination of reperfusion period. In Ber + I/R group, pancreatic vascular congestion and decreased plasma level of insulin were improved concomitant to increase in plasma creatinine and urea nitrogen being smaller than those of the non-treated rats. Berberine exhibited an ameliorative effect on the pancreas against RIR-induced damages. Conclusion: RIR injury has some roles in the development of tissue damages and probably functional disorders of the pancreas in rats. Furthermore, berberine has an ameliorative effect against organ injury induced by RIR in rat.
Farshad Alizadeh Mansouri, Fereshteh Motamedi, Fereshteh Fathollahi, Nafiseh Atapour, Saeed Semnanian,
Volume 1, Issue 1 (Spring and Summer 1997)
Abstract

The effects of chronic morphine administration on the development of long-term potentiation (LTP) were investigated at the Schaffer collateral-CA1 pyramidal cell synapses of the rat hippocampal slices using primed-bursts tetanic stimulation. Significant enhancement of orthodromic population spike (OPS) was found for all stimulus intensities after tetanic stimulation. OPS enhancement was greatest when tested with low to mid-range stimulus intensities (25, 50 and 100 µA). There was also significant decrease in OPS delay. These responses were similar in slices from both control and morphine dependent rats. At all delivered stimulus intensities, the amount of LTP of OPS in slices from dependent rats was larger than that of control slices. However, these differences in LTP of OPS were significant at low stimulus intensities. These findings suggest that chronic morphine administration had induced changes in CA1 neurocircuitry which modulated synaptic plasticity during high frequency stimulation and appeared as augmented LTP and also inhibition of LTP decay.
Farshad Alizadeh Mansouri, Fereshteh Motamedi, Fereshteh Fathollahi, Nafiseh Atapour, Saeed Semnanian,
Volume 1, Issue 1 (Spring and Summer 1997)
Abstract

  The effects of chronic morphine administration on the development of long-term potentiation (LTP) were investigated at the Schaffer collateral-CA1 pyramidal cell synapses of the rat hippocampal slices using primed-bursts tetanic stimulation. Significant enhancement of orthodromic population spike (OPS) was found for all stimulus intensities after tetanic stimulation. OPS enhancement was greatest when tested with low to mid-range stimulus intensities (25, 50 and 100 µ A). There was also significant decrease in OPS delay. These responses were similar in slices from both control and morphine dependent rats. At all delivered stimulus intensities, the amount of LTP of OPS in slices from dependent rats was larger than that of control slices. However, these differences in LTP of OPS were significant at low stimulus intensities. These findings suggest that chronic morphine administration had induced changes in CA1 neurocircuitry which modulated synaptic plasticity during high frequency stimulation and appeared as augmented LTP and also inhibition of LTP decay.


Fereshteh Motamedi, Ali Pourmotabbed, Yaghub Fathollahi, Farshad Alizadeh Mansouri, Saeed Semnanian,
Volume 1, Issue 2 (Fall and Winter 1997)
Abstract

  The involvement of NMDA receptors and voltage-dependent calcium channels in augmentation of long-term potentiation (LTP) was investigated at the Schaffer collateral CA1 pyramidal cell synapses in hippocampal slices of morphine dependent rats, using primed-burst tetanic simulation. The amplitude of the population spike and its delay were measured as indices of increase in postsynaptic excitability. D,L-APV and nifedipine were used as an NMDA receptor antagonist and a voltage-dependent calcium channel blocker, respectively. The amount of LTP of the orthodromic population spike (OPS) was higher in slices from dependent rats. Perfusion of slices from control and dependent rats with ACSF containing D,L-APV (25 µ M) and delivering tetanic simulation showed that D,L- APV completely blocked the LTP of OPS in slices from both control and dependent rats, while nifedipine (10 µ M) attenuated the amount of LTP of OPS in dependent slices and had no effect on controls. The results suggest that the enhanced LTP of OPS in the CA1 area of hippocampal slices from morphine-dependent rats is primarily induced by NMDA receptor activity, and the voltage-dependent calcium channels may also be partially involved in this phenomenon.


Mozhdeh Mansouri, Homayoun Khazali,
Volume 12, Issue 2 (Summer 2008)
Abstract

Introduction: Previous studies have shown that ghrelin inhibits the activity of Hypothalamus –Pituitary – Thyroid (H–P-T) axis. It is also proved that ghrelin increases appetite via Agouti Related Protein and neuropeptide Y pathway, decreases T3 & T4 secretion and inhibits serotonin release from hypothalamic synaptosomes. Serotonin may interact with ghrelin in control of thyroid hormones secretion. Thus, the goal of this study was to determine the influence of the interaction between ghrelin and serotonin agonist on thyroid hormones concentration. This is a suugestive mechanism to determine the effect of serotonin agonist in decreasing the effect of ghrelin. Methods: Twenty four male Wistar rats weighing 230-250 g were randomly divided into 3 groups. The groups respectively received 5 nmol ghrelin ,20 nmol serotonin agonist (R)-8-OH-DPAT or 5 nmol ghrelin with 20 nmol (R)-8-OH-DPAT in the volume of 5μl during 3 days via lateral cerebral ventricle. The blood samples were collected from one day before to one day after injections and brain slices were taken to ensure the place of the canulae is right. The plasma were analysed by Radio Immuno Assay technique to determine T3 and T4 concentrations. Results: The results of this experience showed that the (.i.c.v) injection of ghrelin and (R)-8-OH-DPAT respectively decreased and increased the mean plasma concentrations of thyroid hormones significantly (p<0.05), while the interaction of these two substances showed that (R)-8-OH-DPAT can decease the inhibitory effect of ghrelin on thyroid hormones concentration, but this effect is not statistically significant. (p<0.05) Conclusion: This study showed that ghrelin decreased mean plasma concentration of T3 & T4 significantly and serotonin agonist while injected with ghrelin , because of the stronger effect of ghrelin, could not significantly inhibit this effect of ghrelin. (p<0.05)
Hamid-Reza Mohammadi-Motlagh, Kamran Mansouri, Ali Mostafaie,
Volume 14, Issue 3 (Fall 2010)
Abstract

Introduction: Angiogenesis, the process of new blood vessel formation from pre-existing vessels, has important physiological roles in embryonic development, female reproduction cycle, and wound healing. It is also crucial for pathological processes in several diseases especially tumor growth and metastasis. Thereby, inhibition of angiogenesis as an addition to the conventional therapies such as chemotherapy and radiotherapy has attracted the attention of scientists. Results: Different studies have shown that botanical derivatives specifically antagonize new vessel formation in tumors without significant toxicity to normal tissues and without major adverse reactions. Furthermore, many studies have revealed that the active ingredients of these natural products inhibit tumor cell proliferation through interference with other physiological pathways such as intracellular signaling pathways. A number of studies have also demonstrated that many traditional foods especially plant derived foods have preventive potential against around one third of cancers. Therefore, plant rich diet can inhibit the progression of many chronic diseases such as malignant solid tumors which are related to angiogenesis.

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