Impact of loganin on pro-inflammatory cytokines and depression- and anxiety-like behaviors in male diabetic rats

Behavioral disturbances are observed in most patients suffering from diabetes. According to some evidence, pro-inflammatory cytokines have a key role both in diabetes and behavioral disorders, such as anxiety and depression. In this study, the effect of chronic administration of loganin, as a bioflavonoid, was investigated on pro-inflammatory cytokines and depression- and anxiety-like behaviors in streptozotocin-induced diabetes in male Wistar rats. Blood levels of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were assessed by enzyme-linked immunosorbent assay method. Depression- and anxiety-like behaviors were evaluated by forced swimming test (FST), elevated plus maze (EPM), and open field test (OFT), respectively. Body weight was also measured before the interventions and after the experiments in all groups. Our findings show that loganin-treated animals had significantly lower serum concentrations of IL-6 and TNF-α compared with the diabetic group. In the EPM test, loganin treatment significantly increased the percentage of the open arm time and open arm entries. Moreover, loganin treatment significantly decreased the grooming time and restored distance traveled and center crossing in the OFT. However, it decreased immobility time in the FST. Loganin treatment also significantly restored body weight gain and attenuated blood glucose changes in the diabetic rats. These results indicate that loganin possibly alleviates depression- and anxiety-like behaviors associated with diabetes through lowering the blood glucose and pro-inflammatory cytokine levels. More research is required to show the exact mechanism of antidepressant and anxiolytic effects of loganin in diabetes

The role of hepcidin in chronic mild stress-induced depression

Depression is one of the most prevalent challenges of mental conditions. Yet its exact etiology has not been clear. Chronic stress increases the production of cytokines, which can lead to depression. Hepcidin, an iron modulator, is involved in the inflammation process as well as iron homeostasis. This study was designed to investigate the role of hepcidin, on stress-induced depression. 60 male wistar rats were entered the experiment. We used a chronic unpredictable mild stress (for 28 days) as a rat model of depression. In stressed group, three subgroups were treated with three different doses of dalteparin (a hepcidin inhibitor): 70. IU/kg, 100. IU/kg and 140. IU/kg daily, for 4 weeks. The animals in the stressed group had more depressive-like behavior than the control group. Moreover, chronic mild stress produced an increased serum interleukin-6 levels. These effects were accompanied by an obvious increase in hepcidin mRNA level and iron content in the hippocampus. These changes were blocked by the injection of dalteparin. In conclusion, inhibition of hepcidin may reduce many pathological changes seen in stress-induced depressive disorders. © 2015 Elsevier Ireland Ltd

Effect of chronic mild stress on the expression of hepcidin gene in hippocampus of male rats

Background and Objective: The first effect of stress on the immune system is usually a rapid increase in function which manifests itself by an increase in the number of inflammatory cytokines in blood. It is however, followed by a decrease of function in immunological response. During inflammation, the expression of hepcidin gene is increased in order to keep iron away from pathogens. This study was conducted to determine the effect of chronic mild stress on the expression of hepcidin gene in the hippocampus of the male adult rats. Materials and Methods: This experimental study was carried out on 30 adult male Wistar rats, weighing approximately 200-250 grams. They were randomly allocated into two groups of 15 rats: control and chronic mild stress group. Animals in intervention group were exposed to chronic mild stress for 3 weeks. At the end of the stress protocol, 2 ml blood sample was collected to measure the serum concentration of IL-6. Real time PCR method was used to investigate hepcidin expression in hippocampus. Data were analyzed using SPSS-16 and independent t-test. Results: The mean level of IL-6 was significantly higher in the CMS exposure group (27.98±0.84 pg/ml) than control group (18.29±1.18 pg/ml) (P<0.05). Hepcidin expression in the hippocampus of intervention group was significantly higher (2.69±0.226%) in compared to control group (1±0.105) (P<0.001). Conclusion: This study showed that chronic mild stress increases the expression of hepcidingene and the serum level of IL-6 in adult rats

Immune system and new avenues in Parkinson's disease research and treatment

Parkinson's disease (PD) is a progressive neurological disorder characterized by degeneration of dopaminergic neurons in the substantia nigra. However, although 200 years have now passed since the primary clinical description of PD by James Parkinson, the etiology and mechanisms of neuronal loss in this disease are still not fully understood. In addition to genetic and environmental factors, activation of immunologic responses seems to have a crucial role in PD pathology. Intraneuronal accumulation of alpha-synuclein (alpha-Syn), as the main pathological hallmark of PD, potentially mediates initiation of the autoimmune and inflammatory events through, possibly, auto-reactive T cells. While current therapeutic regimens are mainly used to symptomatically suppress PD signs, application of the disease-modifying therapies including immunomodulatory strategies may slow down the progressive neurodegeneration process of PD. The aim of this review is to summarize knowledge regarding previous studies on the relationships between autoimmune reactions and PD pathology as well as to discuss current opportunities for immunomodulatory therapy

Rosa canina L. methanolic extract prevents heat stress-induced memory dysfunction in rats

NEW FINDINGS: What is the central question of this study? Heat stress has harmful effects on the brain structure and synaptic density via induction of oxidative stress and neuroinflammation, which result in neuronal damage in the hippocampus and thereby cognitive impairments. In this study, we investigate the effect of Rosa canina treatment on cognitive function in heat stress-exposed rats and its underlying mechanisms. What is the main finding and its importance? We show that R. canina improves cognitive deficits induced by heat stress by attenuation of oxidative stress and neuroinflammation and by upregulation of synaptic proteins in the hippocampus. ABSTRACT: The aim of the study was to evaluate the effects of aqueous methanolic extract of Rosa canina (RC) dried fruits on oxidative stress, inflammation, synaptic degeneration and memory dysfunction induced by heat stress (HS) in rats. Sixty adult male Wistar rats were randomly divided into five groups as follows: the control group received normal saline (NS); the HS group was exposed to heat stress (43 degrees C) for 15 min once a day for 2 weeks; and HS+R groups were exposed to heat stress and received one of three doses (250, 500 or 1000 mg kg(-1) ) of RC methanolic extract for 2 weeks. A passive avoidance test and a Y-maze test were performed to assess learning and memory. The levels of reactive oxygen species were assessed. The serum cortisol concentration and hippocampal total antioxidant capacity, superoxide dismutase and glutathione peroxidase were also detected using spectrophotometry. The protein expressions of c-Fos, heat-shock protein-70, tumour necrosis factor-alpha, growth-associated protein 43, post-synaptic density-95 and synaptophysin were evaluated in the hippocampal tissue. The results showed that RC significantly improved cognitive dysfunction induced by HS, which was accompanied by downregulation of tumour necrosis factor-alpha and upregulation of growth-associated protein 43 and synaptophysin proteins in the hippocampus of HS-exposed rats. Furthermore, RC significantly attenuated serum cortisol concentrations and upregulated heat shock protein-70 and c-Fos in the hippocampus. In addition, the administration of RC attenuated reactive oxygen species levels and enhanced antioxidant defense in the hippocampus. These findings indicate that RC attenuated the deleterious effect of HS on cognition through its antioxidant properties and by enhancing synaptic function and plasticity