In the present study, we have investigated the effects of silymarine on depression and the possible role of serotonergic system in these effects. The rats were anesthetized intraperitoneally with ketamine hydrochloride and placed in a Stoelting stereotaxic instrument. A stainless steel guide cannula (22-gauge) was implanted in the third ventricular region. The third ventricular region was infused by means of an internal cannula (27-gauge), terminated 1 mm below the tip of the guide cannula. Forced swimming test was used for evaluating the depression. The results obtained from this study showed that oral administration of silymarin (35, 70, 140 and 280 mg/rat) for two weeks increased the immobility time in forced swimming test, indicating an increase in depression level of the treated rats. Intra-third-ventricle (Intra-TV) infusion of 5HT1A receptor agonist 8-OH-DPAT (25 and 10 ng/rat) decreased the immobility time indicating an anti-depression effect, while injection of 5HT1A receptor antagonist NAN190 (0.25, 0.5 and 1 μg/rat) had no significant effect on immobility time. An effective dose of 8-OH-DPAT (10 ng/rat) co-administered with silymarin (140 and 280 mg/rat) decreased the depressogenic effects of silymarin. These results showed that the depressogenic effects of silymarin may be modulated via 5HT1A receptor of serotonin.
Decreased level of the anti-inflammatory adipokines, secreted frizzled-related protein 5 and adiponectin, in high cholesterol diet-induced atherosclerotic rats
In the present study, the effects of prenatal stress on spatial learning and memory deficit and its relationship with hippocampal insulin resistance were examined in male and female offspring.Female NMRI mice were mated with males overnight, and the 0-day of pregnancy was detected (Gestational day 0-GD0). The pregnant mice were then randomly divided into stress and control groups. The stress group received stress from the GD0 to GD10. On post natal day 30 (PND30), the offspring were divided into 4 subgroups, namely: male-control, female-control, male-stress, and female-stress. Barnes maze method was used for spatial learning evaluation. Plasma cortisol and insulin levels were measured at the beginning of the experiments. At the end of the experiments, the animals' brains were removed, and their hippocampus was extracted. The hippocampus was homogenized, and its insulin and insulin-receptor contents were evaluated.The stressed animals needed more time for reaching to target hole. In addition, they spend more distance to find the target hole, which was more pronounced in the male offspring. Both plasma and hippocampal insulin content were reduced in the stressed groups. Moreover, the hippocampal insulin receptors protein was reduced in the stressed animals. There was a positive relationship between plasma and hippocampal content and memory deficit in the stressed groups.These results indicated that prenatal stress could induce spatial learning and memory deficit in offspring, which is associated with plasma and hippocampal insulin and receptor content reduction (hippocampal insulin resistance) in these animals.Maternal stress is very harmful for fetus.The effect of stress is significant during the early days of gestation.This effect is due to several hormonal and neuronal disturbances including Insulin resistance.The effects of stress on the fetus is gender dependent.The possible effectiveness of prenatal stress on learning and memory in neonates and also the changes in hippocampus as of essential part of the brain involved in learning and memory. We found that prenatal stress can reduce the insulin effects in hippocampus and it may be the main cause of stress on neonatal memory deficits.
Background: Glucose is an essential element in the supply of body’s energy. In diseases such as diabetes, glucose increase is associated with disturbance in metabolism. Cortisol is an important hormone in the regulation of glucose metabolism, and human serum albumin (HSA) is one of the most important glucose and cortisol transmitters in blood. Interaction between albumin and these ligands could affect HSA secondary structure and its stability. Objectives: The aim of this study was to investigate HSA secondary structure in the presence of different concentrations of glucose and cortisol. Methods: This was an in vitro (analytical/descriptive) study in which, completely randomized design was used to study the interaction between human serum albumin at 37°C at different glucose concentrations of 0, 80, 180, 240, and 400 mg/dL and cortisol at concentrations of 0, 10, 20, and 40 µg/dL. Intrinsic fluorescence spectroscopy and Circular dichroism (CD) were performed to obtain data. Results: HSA secondary structure underwent changes in the presence of different concentrations of cortisol and glucose. P values less than 0.01 were considered to be statistically significant. Fluorescence spectroscopy and CD results showed that at normal glucose concentrations, HSA was very flexible, beta-sheet content reduced, and the maximum increase in fluorescence and blue-shift happened. At higher concentrations of glucose, HSA became rigid. Also, HSA in presence of 10 µg/dL cortisol was very flexible; but a cortisol concentration of 40 µg/dL caused stability in HSA structure in presence of different glucose concentrations. Conclusions: Under normal glucose conditions, very low cortisol concentrations create large changes in HSA secondary structure. At normal glucose concentrations, some of the binding sites of HSA that are all occupied by glucose at higher concentrations become available to cortisol. Cortisol structure is very hydrophobic, which causes large changes in HSA secondary structure and significant increases in quenching and blue shift. In conclusion, binding of compounds such as medicines to HSA sites may be affected by competitive bindings of glucose, depending on its concentration in the blood.
Alzheimer's disease is a neurodegenerative disorder characterized by accumulation of amyloid beta in the hippocampus. In recent decades, herbal medicine has been widely used to treat many neurodegenerative disorders,as in comparison to conventional drugs, herbal remedies exert minimal side effects. Here, the effects of thymoquinone, as the main active component of
The liver as a highly metabolic organ, has a crucial role in human body. Its function is often impressed by changes of the blood flow, hypovolemic shock, transplantation, etc. Maintaining liver function is a major challenge and there are many approaches to potentiate this organ against different stresses. Antioxidants protect organs against oxidative stress. P-coumaric acid (PC) as an oxidant has many beneficial effects. Therefore, PC was used as a pretreatment to test its potential against oxidative stress induced by liver Ischemia-reperfusion injury in rats.In order to test the potential hepatoprotective effect of PC against IR injury, five groups of rats were used: Normal (NC; intact group); Sham; p-coumaric acid (PC); IR-CO, and PC-IR. PC, Sham, NC, PC-IR and IR-CO groups that received vehicle or p-coumaric acid at a dose of 100 mg/kg for 7 consecutive days as pretreatment before IR induction. Animals in PC-IR, and IR-CO groups underwent hepatic IR injury. Liver levels of antioxidants were determined and functional liver tests were done. Hematoxylin and eosin staining was done to determine the structural changes of the liver. Gene expression of caspase-3 was also assessed.Hepatic IR injury disrupted liver function by increasing the levels of AST, and ALT, and decreasing GSH, SOD and catalase. PC significantly decreased liver inflammation, reverted liver functional enzymes and antioxidants levels to normal, reduced the gene expression of caspase-3 in PC-IR rats compared to the IR-CO group.These findings revealed that PC through improving liver´s antioxidants, liver functional tests and down-regulating apoptotic gene protein, caspase-3, protects the liver against injury induced by IR.
Background: Chronic complications (e.g. cardiovascular failure) are among the most common problems in diabetics. It is suggested that oxidative stress and lipid peroxidation play a key role in chronic diabetic complications. Supplementation with agents containing antioxidant properties can suppress lipid peroxidation. Many studies confirmed the antioxidant properties of zinc in biological systems. The aim of the present study was to evaluate the effect of zinc supplements on serum lipid oxidizability in diabetic patients. Materials and Methods: In this clinical trial study, 60 diabetic patients were chosen and randomly divided into two groups. Serum lipid oxidizability and serum zinc level were evaluated in each group before and after zinc supplementation (25.50 mg/day for 2 month). Lipid oxidizability was followed through monitoring the change of conjugated compounds in diluted serum after adding Cu 2+ by spectrophotometric method. S erum zinc level was measured by atomic absorbance spectrophotometer. Results: While there was no significant change in the post- supplementation zinc level (25 mg) in the first group, zinc serum level was increased significantly (p Conclusion: Our results indicate that zinc supplementation (25.50 mg) in short period of time has no favorable effect on serum lipid oxidizability in diabetic patients. It seems that zinc dose, duration of treatment and also the patients' condition may affect their response to supplementation.
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