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The benefits of exercise in TBI have been proven. However, the time-dependent effects of exercise initiation and the involved mechanisms are controversial. We investigated the effects of preconditioning, continuous, early, and delayed treadmill exercise on motor behavior, brain edema, inflammation, and oxidative stress in experimental traumatic brain injury (TBI).48 male rats were assigned into two groups: sedentary control (Sham and TBI) and exercise groups: 1MB (preconditioning, initiation beginning at 1 month before trauma), 1MBA (continuous, initiation beginning at 1 month before and continuing 1 month after trauma), 24hA (early, initiation beginning at 24 h after trauma), and 1WA (delay, initiation beginning at 1 week after trauma). The rats in exercise groups were forced to run on a treadmill five days a week for 30 min per day. Rotarod and open file were used to assess motor behavior. ELISA was also used to measure total antioxidant capacity (TAC), tumor necrosis factor-alpha (TNF-α), and malondialdehyde (MDA) in serum and CSF.Exercise significantly decreased neurological impairments, motor deficits, and apoptosis compared with the sedentary group. Early (within 24 h) and ongoing (1 MBA) exercise significantly improved motor behavior after TBI. In addition, these exercise programs inhibited brain edema and the number of apoptotic cells. MDA and TNF-α levels increased in all exercise groups, but the effects were greater after early exercise than after delayed exercise, resulting in a significant decrease in TAC levels in serum and CSF. We discovered a positive correlation between MDA, TAC, and TNF-α concentration in serum and CSF.Our finding suggests that early exercise (24hA) and 1MBA groups afford neuroprotection and reduce the second injury consequence, probably by reducing neuronal apoptosis and oxidative stress.

INTRODUCTION The aim of this study was to determine the anti-inflammatory effect of female sex hormones on the level of intracellular molecules of cytokine signaling pathway after diffuse traumatic brain injury (TBI) in ovariectomized rats. METHODS Female rats were divided into 10 groups: control, sham, TBI, Vehicle (oil), Vehicle E1 (33.3 µg/kg), E2 (1 mg / kg), P1 (1.7 mg/kg), P2 (8 mg / kg), E2 + P1. All drugs were injected 0.5 h after TBI. Brain edema and the brain levels of P-STAT-3, NFκB-P52, NFκB-P65, P-IκB, and SOCS-3 by immunohistochemistry measured at 24 h after TBI. RESULTS Increased brain edema after TBI was inhibited by different doses of estrogen, progesterone (P

Background: Jaundice is one of the most common diseases of the infancy period. It could be caused by different factors, including infections such as the urinary tract. The present study aims to evaluate the prevalence and causes of urinary tract infection in newborns. Materials and Methods: The present work is a cross-sectional study conducted on 100 newborns with jaundice hospitalized at the neonatal ward of the Pasteur Hospital of Bam or referred to its outpatient clinic. Participants were selected through convenient sampling. Besides the routine tests for jaundice, a urine sample was also taken from the newborns for culturing and evaluating urinary tract infection. After collecting the data, they were analyzed using the chi-square and t-tests. Results: According to the results, 41 (41) of the newborns were girls, and 59 of them (59) were boys. The prevalence of urinary tract infection among newborns with jaundice was 27. The most common cause of infection was Escherichia Coli, and the rate of infection was lower among newborns breastfed compared to those fed by infant formula (p

This study assessed the effects of single or combined administration of temozolomide (TMZ) and interferon-gamma (IFN-ᵞ) on anxiety-like behaviors, balance disorders, learning and memory, TNF-α, IL-10, some oxidant and antioxidants factors with investigating the toll-like receptor-4 (TLR4) and p-CREB signaling pathway in C6-induced glioblastoma of rats.40 male Sprague-Dawley rats bearing intra-caudate nucleus (CN) culture medium or C6 inoculation were randomly divided into five groups as follows: Sham, Tumor, TMZ, IFN-ᵞ and a TMZ + IFN-ᵞ combination. The open-field test (OFT), elevated plus maze (EPM), rotarod, and passive avoidance test (PAT) were done on days 14-17. On day 17 after tumor implantation, brain tissues were extracted for histopathological evaluation. TNF-α, IL-10, SOD, GPX, TAC, MDA, the protein level of TLR4 and p-CREB was measured.Combination therapy inhibited the growth of the tumor. Treatment groups alleviated tumor-induced anxiety-like behaviors and improved imbalance and memory impairment. SOD, GPX, and TAC decreased in the tumor group. The combination group augmented GPX and TAC. MDA decreased in treatment groups. TMZ, IFN-ᵞ reduced tumor-increased TNF-α and IL-10 level. The combination group declined TNF-α level in serum and IL-10 level in serum and brain. Glioblastoma induced significant upregulation of TLR4 and p-CREB in the brain which inhibited by IFN-ᵞ and TMZ+ IFN-ᵞ.The beneficial effects of TMZ, IFN-ᵞ, and TMZ+ IFN-ᵞ on neurocognitive functioning of rats with C6-induced glioblastoma may be mediated via modulating oxidative stress, reduced cytokines, and the downregulation of expression of TLR4 and p-CREB. Combination treatment appears to be more effective than single treatment.

Aim Traumatic Brain Injury (TBI) is widely acknowledged as a significant risk factor for death and disability. Our goal in this experiment was to see if Auraptene (AUR) could help rats recover from TBI-induced disability by measuring of oxidative stress parameters. Material and methods Adult male Wistar rats were randomly assigned to one of six groups: sham, TBI, Vehicle (DMSO), TBI+ AUR (4 mg/kg), TBI + AUR (8 mg/kg), TBI + AUR (25 mg/kg). The animals were anesthetized. After that, diffuse TBI was done by Marmarou model in male rats. Then, the brain tissues were harvested. Some of oxidative stress parameters, and TNFα levels were evaluated. Results TBI-induced brain damage was significantly inhibited by AUR (25 mg/kg), as evidenced by decreased Malondialdehyde (MDA) and Nitric Oxide (NO) levels, oxidative stress inhibition and reduced levels of pro-inflammatory cytokine tumor necrosis factor (TNF-α) in the brain. Conclusion This study showed that probably the AUR prevents complications of TBI through decreases in brain edema, modulating oxidative stress, and reductions in the levels of inflammatory cytokines.

It has been shown that 17β-estradiol (E2) hormone is an essential biological factor for increasing the sensitivity of women to drug abuse. Recent studies have shown a potential overlap between the molecular pathways of cannabinoids and ovarian hormones. The current study evaluated the interference between the marijuana and E2 effect on spatial learning and memory and the role of the G protein-coupled estrogen receptor (GPR30) in young female rats. The animals were separated into two main groups: intact-ovary and ovariectomized (OVX) rats. The latter group received intraperitoneal injections of E2, G-1 (GPR30 agonist), G-15 (GPR30 antagonist), marijuana, and different combinations of these substances for 28 days. Spatial learning and memory were evaluated by the Morris water maze (MWM) test. We also assessed the BDNF (brain-derived neurotrophic factor) concentration and the hippocampal level of GPR30. The results showed a significant reduction of spatial learning and memory in OVX rats compared to intact-ovary rats, which were restored by E2 replacement. Moreover, treatment with G-1 mimicked E2 effects on spatial learning and memory. Marijuana impaired spatial learning and memory in intact-ovary rats, while improved in OVX rats. We also found that treatment with M + E2 induced significant impairment in spatial learning and memory; however, treatment with M + G1 and M + G15 + E2 showed no significant difference. No significant differences in BDNF expression were observed in experimental groups. These results suggest that marijuana and E2 interact in their effect on spatial learning and memory in young female rats, but GPR30 seems to play no role in this interaction.

Several studies have shown that 17β-estradiol (E2) exerted beneficial effects on liver disease, and it has a protective impact on brain damage after traumatic brain injury (TBI). TBI-induced liver injury is associated with the activation of TLR4. However, it remains unknown whether E2 can modulate TBI-induced liver injury through TLR4. The objective of this study was to determine the role of TLR4 in hepatoprotective mechanisms of E2 after TBI. Diffuse TBI induced by the Marmarou model in male rats. TAK-242 as a selective antagonist of TLR4 (3 mg/kg) and E2 (33.3 μg/kg) were injected (i.p) respectively 30 min before and 30 min after TBI. The results showed that E2 and TAK-242 markedly inhibited TBI-induced liver injury, which was characterized by decreased aminotransferase activities, inhibition of the oxidative stress, and reduced levels of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and IL-17 in the liver. We also found that TBI induced significant upregulation of TLR4 in the liver, with peak expression occurring 24 h after TBI, and that treatment with E2 significantly inhibited the upregulation of TLR4. Also, both classic [Estrogen receptors alpha (ERα) and beta (ERβ)] and non-classic (G protein-coupled estrogen receptor GPER) E2 receptors are involved in modulating the expression of TLR4. These results suggested that the hepatoprotective effects of estradiol after TBI may be mediated via the downregulation expression of TLR4.

Brain edema and increased intracranial pressure (ICP) are among the main causes of neurological disturbance and mortality following traumatic brain injury (TBI). Since pregabalin neuroprotective effects have been shown, this study was performed to evaluate the possible neuroprotective effects of pregabalin in experimental TBI of male rats. Adult male Wistar rats were divided into 4 groups: sham, vehicle, pregabalin 30 mg/kg and pregabalin 60 mg/kg. TBI was induced in vehicle and pregabalin groups by Marmarou method. Pregabalin was administered 30 min after TBI. Sham and vehicle groups received saline. Brain water and Evans blue content and histopathological changes were evaluated 24, 5 and 24 h after TBI, respectively. The ICP and neurological outcomes (veterinary coma scale, VCS) were recorded before, 1 h and 24 h post TBI. The results showed a significant reduction in brain water content and ICP, and a significant increase in VCS of pregabalin group (60 mg/kg) as compared to vehicle group (P 0.05). Also, pregabalin reduced brain edema and apoptosis score as compared to vehicle group. Post TBI pregabalin administration revealed a delayed but significant improvement in ICP and neurological outcomes in experimental TBI. The underlying mechanism(s) was not determined and needs further investigation.

The role of aquaporin-4 (AQP4) and interleukin-6 (IL-6) in the development of brain edema post-traumatic brain injury (TBI) has been indicated. The present study was designed to investigate the effect(s) of administration of progesterone (P) and/or estrogen (E) on brain water content, AQP4 expression, and IL-6 levels post-TBI. The ovariectomized rats were divided into 11 groups: sham, one vehicle, two vehicles, E1, E2, P1, P2, E1 + P1, E1 + P2, E2 + P1, and E2 + P2. The brain AQP4 expression, IL-6 levels, and water content were evaluated 24 h after TBI induced by Marmarou’s method. The low (E1 and P1) and high (E2 and P2) doses of estrogen and progesterone were administered 30 min post-TBI. The results showed that brain water content and AQP4 expression decreased in the E1, E2, P1, and P2-treated groups. The administration of E1 decreased IL-6 levels. Addition of progesterone decreased the inhibitory effect of E1 and E2 on the accumulation of water in the brain. Administration of E1 + P1 and E1 + P2 decreased the inhibitory effect of E1 on the IL-6 levels and AQP4 protein expression. Our findings suggest that estrogen or progesterone by itself has more effective roles in decrease of brain edema than combination of both. Possible mechanism may be mediated by the alteration of AQP4 and IL-6 expression. However, further studies are required to verify the exact mechanism.

Our previous studies have demonstrated that estrogen is protective in traumatic brain injury (TBI). However, concerns about negative consequences of estrogen therapy have led to find other strategies to obtain estrogen’s benefits in the brain, including the use of a soy diet. This study was designed to determine whether a soy diet is protective in TBI. The male Albino N-Mary rats received either a soy- free diet (SFD) or soy diet (SD) from weaning to adulthood. The SFD and SD rats were separately divided to two groups of sham and TBI (n= 18 in each group). The diffuse and severe brain injury was induced by Marmarou method. The disruption of Blood brain- barrier (BBB) was evaluated 48 h post- TBI. The intracranial pressure (ICP), the neurologic outcome, and the beam-walk task (WB) were determined before trauma, on trauma day (D0), and first (D1) and second (D2) days post- TBI. Evans blue dye was significantly high in the SFD + TBI group vs. other groups. The ICP was significantly high in the SFD + TBI group in all times evaluated, and in the SD + TBI group on D1 and D2, however lower than that in the former group. The neurologic outcome score was significantly low in the SFD + TBI group vs. the sham groups in all times. Also the traversal time in WB task was significantly high in the SFD + TBI group not the SD + TBI group, vs. the sham groups in all times, however significant difference of distance traveled was shown only on trauma day. The results of this study demonstrate that soy diet can prevent the disruption of BBB, and attenuate the elevation of ICP, and the disturbance of vestibulomotor and neurologic performance in TBI.

Background The role of transient receptor potential vanilloid 1 (TRPV1) in peripheral nervous system has been studied well but its role in the central nervous system remains to be studied in detail. The expression of TRPV1 receptors in hippocampus is suggesting that they may play an important role in higher cognitive functions such as learning and memory. Methods In the present study, the role of TRPV1 receptors in acquisition and retrieval of spatial memory of male Wistar rats was evaluated by intra-ventral hippocampus administration of TRPV1 selective agonist (OLDA) and antagonist (AMG9810) using Morris water maze. Results The results demonstrated that administration of either OLDA (0.001, 0.01 and 0.1 μg/rat) or AMG9810 (0.003, 0.03 and 0.3 μg/rat) did not influence memory acquisition or retrieval. Conclusions These data suggest that ventral-hippocampal TRPV1 receptors possibly are not involved in spatial learning and memory.