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Uteroplacental insufficiency (UPI) causes neurodevelopmental deficits in the brain of intrauterine growth-restricted offspring, even though the mechanisms are equivocal. The most important factor in these deficits is oxidative stress. Cinnamic acid (CA) and derivatives have been described to exhibit antioxidant activity. In this study, the researchers examined the neuroprotective effect of CA on the parameters of oxidative stress and hippocampal cell density in the UPI rat model. In this experiment, the Wistar rats were mated, and UPI was induced at gestation day (GD) 18. For UPI induction, anterior uterine artery occlusion surgery is conducted in deep anesthesia. From GD15, CA was administrated orally in 25, 50, and 100 mg/kg BW doses until GD21. GD21 evaluated the weight of the uterine, placenta, and embryo. Also, the oxidative stress parameters in the hippocampus, e.g., catalase activity (CAT), total antioxidant activity (TAC), and malondialdehyde (MDA), were measured using the ELISA technique in the fetus. Finally, the cell density of the fetal hippocampus was estimated using the histopathological method. CA reduces the MDA at various concentrations and increases CAT and TAC in comparison with the untreated group (p ˂ 0.001). Besides, the cell density of CA3 and CA4 as hippocampus subareas are significantly increased than the untreated group, especially in the UPI + CA100 group (p = 0.002 and p = 0.001, respectively). Our data revealed that CA ameliorated the oxidative stress parameters and hippocampal cell damages in the UPI rats. Therefore, the CA can have neuroprotective effects in UPI model.

Hormonal disorders, oxidative stress, and inflammation in ovarian tissue cause ovulation failure in women with polycystic ovary syndrome. Considering the antioxidant properties of gallic acid (GA), the aim of this study was to investigate the effect of GA on pro-inflammatory cytokines, antioxidant enzyme activity, and DNA oxidative damage of ovarian tissue in a rat model of estradiol-induced polycystic ovary (PCO). In this experimental study, 32 female Wistar rats were divided into four groups. These included control (saline solution, orally), PCO+saline (estradiol valerate + saline solution, orally), PCO+GA50, and PCO+GA100 (estradiol valerate +50 and 100 mg/kg gallic acid, orally), respectively. The PCO model was induced by a single intramuscular injection of estradiol valerate (EV, 4 mg/kg). Twenty-four days after PCO modeling, tissue concentration of tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) and also the activity level of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), malondialdehyde (MDA), and 8-oxo-2′-deoxyguanosine (8-OHdG) in ovarian tissue were measured through ELISA technique. Compared with the PCO+saline, in the GA-treated group, the concentration of TNF-α, IL-1β, and IL-6 in a dose-dependent manner significantly decreased (p > 0.05). In addition, the activity level of SOD, CAT, and GPX enzymes significantly increased (p 0.05) in a dose-dependent manner. GA is an anti-inflammatory and an antioxidant polyphenol which reduces the concentration of inflammatory cytokines, oxidative stress, lipid peroxidation, and DNA oxidative damage of ovarian tissue in a rat’s model of PCO.

Among stem cells, mesenchymal stem cells (MSCs) are ideal for practical regenerative medicine and among MSCs, adipose-derived (Ad)-MSCs are the best sources for this regard. Migration or homing to the injured tissue is the main property of MSCs which is related to chemokine receptors on their cell membrane and could be affected by some materials such as valproic acid (VPA). The present study investigated whether VPA could increase the expression of these receptors. In doing so, human Ad-MSCs were isolated from adipose tissue (AT), and after primary culture and characterization, the cells in passage four were primed with 5 mM of VPA for 24, 48, and 72 h. The cells that received no treatment were considered as control group. Then, expressions of chemokine receptors CCR1, CCR7, CX3CR, CXCR4, and CXCR6 were evaluated by PCR and semi-quantitative RT-PCR. GAPDH was considered as an internal control. All of studied chemokine receptors expressed in control group except CCR7 and CX3CR. The expression of CCR1 was low and no detectable increasing after priming with VPA could be seen, but CXCR4 and CXCR6 were significantly overexpressed. Also, the overexpression of these two receptors was time-dependent. We concluded that VPA treatment enhances homing of Ad-MSCs via overexpression of chemokine receptors in these cells, especially CXCR4 and CXCR6 as CXC group of these receptors and this expression is time-dependent, too.

Pathophysiology of depression is a controversial issue. The present study aimed at investigating the pathophysiology of depression in trimethyltin (TMT) intoxication as a hippocampal degeneration inducer. The effect of Lithium Chloride (LiCl) chronic administration on the amelioration of depression symptoms was also investigated. The rats were injected with single dose of TMT (8 mg/kg intra-peritoneal). The three test groups received 20, 40 and 80 mg/kg of LiCl respectively. Likewise, the vehicle treated group received saline for fourteen day. In order to assess the depression level, the immobility time of the rats was measured in the forced swim test (FST) and tail suspension test (TST). Then, the serum levels of tumor necrotic factor alpha (TNF-α) and brain derived neurotrophic factor (BDNF) were measured. Histological methods were then used to determine degenerated neurons and cell density in the hippocampus. An increase in the immobility time in FST and TST was seen in the rats who received TMT, while the rats receiving LiCl showed a significantly decreased immobility. In addition, LiCl administration increased the serum level of BDNF, while it decreased the serum level of TNF –α after TMT intoxication. The number of degenerated neurons in CA1, CA2, CA3 and DG of LiCl-treated groups were lower than that of vehicle treated group. LiCl treatment increased hippocampal cell density, especially in CA3 subfield. Taken together, the findings suggested that chronic administration of Lithium Chloride could ameliorate TMT-induced depression through up-regulation of BDNF and TNF-α signaling pathway.

Trimethyltin as a methylated organotin can induce selective neuronal death in the central nervous system of humans and rodents. On the other hand, lithium has neuroprotective and neurotrophic effects. Therefore, the aim of this study was to evaluate the neuroprotective effects of lithium chloride on neuronal density in the entorhinal cortex of rat brain after trimethyltin intoxication. Thirty male Sprague–Dawley rats were divided into three equal groups: control, trimethyltin (8 mg/kg, single dose, intraperitoneally), and trimethyltin + lithium chloride (single dose of 8 mg/kg of trimethyltin + 20 mg/kg lithium chloride for 14 consecutive days, intraperitoneally). At the end of the experiment, the entorhinal cortex histopathological examination was performed in all rats of each group. Our results showed that the neural density of the entorhinal cortex in trimethyltin and trimethyltin + lithium chloride groups was significantly decreased in comparison to control group in the levels of P